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Organelle symphony:Nuclear factor erythroid 2-related factor 2 and nuclear factor-kappa B in stroke pathobiology 认领 引用 被引量：1
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作者 Ziliang Hu Mingyue Zhao +4 位作者 Hangyu Shen Liangzhe Wei Jie Sun Xiang Gao Yi Huang 《Neural Regeneration Research》 SCIE CAS CSCD 2026年第4期1483-1496,共14页
Strokes include both ischemic stroke,which is mediated by a blockade or reduction in the blood supply to the brain,and hemorrhagic stroke,which comprises intracerebral hemorrhage and subarachnoid hemorrhage and is cha... Strokes include both ischemic stroke,which is mediated by a blockade or reduction in the blood supply to the brain,and hemorrhagic stroke,which comprises intracerebral hemorrhage and subarachnoid hemorrhage and is characterized by bleeding within the brain.Stroke is a lifethreatening cerebrovascular condition characterized by intricate pathophysiological mechanisms,including oxidative stress,inflammation,mitochondrial dysfunction,and neuronal injury.Critical transcription factors,such as nuclear factor erythroid 2-related factor 2 and nuclear factor kappa B,play central roles in the progression of stroke.Nuclear factor erythroid 2-related factor 2 is sensitive to changes in the cellular redox status and is crucial in protecting cells against oxidative damage,inflammatory responses,and cytotoxic agents.It plays a significant role in post-stroke neuroprotection and repair by influencing mitochondrial function,endoplasmic reticulum stress,and lysosomal activity and regulating metabolic pathways and cytokine expression.Conversely,nuclear factor-kappa B is closely associated with mitochondrial dysfunction,the generation of reactive oxygen species,oxidative stress exacerbation,and inflammation.Nuclear factor-kappa B contributes to neuronal injury,apoptosis,and immune responses following stroke by modulating cell adhesion molecules and inflammatory mediators.The interplay between these pathways,potentially involving crosstalk among various organelles,significantly influences stroke pathophysiology.Advancements in single-cell sequencing and spatial transcriptomics have greatly improved our understanding of stroke pathogenesis and offer new opportunities for the development of targeted,individualized,cell typespecific treatments.In this review,we discuss the mechanisms underlying the involvement of nuclear factor erythroid 2-related factor 2 and nuclear factor-kappa B in both ischemic and hemorrhagic stroke,with an emphasis on their roles in oxidative stress,inflammation,and neuroprotection. 展开更多
关键词 inflammation nuclear factor erythroid 2-related factor 2 nuclear factor-kappa B organelles oxidative stress stroke
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Shenling Baizhu powder(参苓白术散)reduced the oxidative stress and mitochondrial damage during ulcerative colitis via the Kelch-like ECH-associated protein 1-NF-E2-related factor 2/nuclear factor kappa B pathway 认领 引用 被引量：1
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作者 ZHANG Quanhui ZENG Jinlan +3 位作者 SU Liang WANG Yi DENG Yongwen ZHANG Xiuchai 《Journal of Traditional Chinese Medicine》 SCIE CAS CSCD 2026年第3期584-593,共10页
OBJECTIVE:To explore the effects and relative mechanisms of Shenling Baizhu powder(参苓白术散,SBP)on ulcerative colitis(UC).METHODS:This study investigates the potential of SBP,a traditional Chinese herbal formula,in ... OBJECTIVE:To explore the effects and relative mechanisms of Shenling Baizhu powder(参苓白术散,SBP)on ulcerative colitis(UC).METHODS:This study investigates the potential of SBP,a traditional Chinese herbal formula,in attenuating inflammation and oxidative stress in UC.Applying both in vivo(rat)and in vitro(human colonic epithelial cells)models,we explored the anti-inflammation and oxidative stress effect of SBP,focusing on the Kelch-like ECHassociated protein 1-NF-E2-related factor 2uclear factor kappa B(KEAP1-NRF2/NF-κB)pathway and mitochondrial homeostasis.RESULTS:Results demonstrated that SBP administration significantly improved the health status of rats,with less intestinal injury,and reduced inflammatory cytokines(tumor necrosis factor-alpha,interleukin-1 beta,and interleukin-6)and oxidative stress(myeloperoxidase,malondialdehyde,and reactive oxygen species)both in vivo and in vitro.Moreover,SBP restored the inhibited KEAP1-NRF2/NF-κB signaling during inflammatory responses induced by dextran sulfate sodium or lipopolysaccharide,and decreased the expression level of the inflammatory molecule:NF-κB.Besides,SBP also helped to restore the mitochondrial dynamics,as evidenced by the recovery of mitochondrial membrane potential and mitofusin-2 levels.CONCLUSION:These findings suggest that SBP may offer a promising alternative therapy for managing UC,providing anti-inflammatory and antioxidant benefits as key molecular mechanisms. 展开更多
关键词 colitis ulcerative inflammation oxidative stress Kelch-like ECH-associated protein 1 NF-E2-related factor 2 NF-kappa B Shenling Baizhu powder
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Tamarixetin suppresses neuronal ferroptosis in ischemic stroke rats by targeting and facilitating nuclear factor erythroid-2-related factor 2 expression 认领 引用
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作者 Yanqiu Yang Mingxia Fang +8 位作者 Qingqi Meng Yan Mi Libin Xu Hua Guo Yueyang Liu Mingzhong Li Nanik Siti Aminah Zipeng Gong Yue Hou 《Acupuncture and Herbal Medicine》 CAS CSCD 2026年第1期73-90,共18页
Objective:Neuronal ferroptosis has emerged as a promising therapeutic target for ischemic stroke.Tamarixetin,a natural dietary flavonoid,exerts protective effects against ischemic stroke by modulating neuroinflammator... Objective:Neuronal ferroptosis has emerged as a promising therapeutic target for ischemic stroke.Tamarixetin,a natural dietary flavonoid,exerts protective effects against ischemic stroke by modulating neuroinflammatory responses and mitigating oxidative stress.However,its potential role in regulating neuronal ferroptosis remains unclear.Methods:A rat model of middle cerebral artery occlusion and reperfusion and an erastin-treated SH-SY5Y cell model were used for in vivo and in vitro experiments,respectively.The neurological function of the rats was evaluated using a series of behavioral tests,the Garcia scoring system,and 2,3,5-triphenyltetrazolium chloride staining.Neuronal damage was detected via immunofluorescence staining and terminal deoxynucleotidyl transferase(TdT)-mediated deoxyuridine triphosphate(dUTP)nickend labeling.Commercial kits,western blotting,and coimmunoprecipitation were used to analyze neuronal ferroptosis and the activation of the Nuclear factor erythroid-2–related factor 2(Nrf2)signaling pathway.The direct target protein of tamarixetin was examined using the cellular thermal shift assay,drug affinity-responsive target stability assay,surface plasmon resonance,and molecular docking.Cellular Nrf2 was knocked down using small interfering RNA.Results:Tamarixetin mitigated the neurological dysfunctions of middle cerebral artery occlusion and reperfusion(MCAO/R)rats,including motor dysfunction,limb coordination impairment,neurological deficit,cerebral infarction,and reduced neuronal loss.Furthermore,it alleviated neuronal ferroptosis in vivo and in vitro by lowering the levels of iron ions,reactive oxygen species,malondialdehyde,and acyl-CoA synthetase long-chain family member 4 and upregulating the expression of superoxide dismutase,glutathione,glutathione peroxidase 4,heme oxygenase-1,and solute carrier family 7 member 11.Tamarixetin activated the Nrf2 signaling pathway by suppressing Keap1 protein expression,weakening the interaction between Keap1 and Nrf2,upregulating Nrf2 protein expression and nuclear translocation,and promoting antioxidant response element activity.Nrf2 is the direct binding protein of tamarixetin.It specifically interacts with amino acid residues at arginine 72,arginine 515,and lysine 518.The effects of tamarixetin on Nrf2 signaling pathway activation and neuronal ferroptosis inhibition were abrogated in Nrf2 knockdown cells challenged with erastin.Conclusions:Our findings not only identify tamarixetin as a novel ferroptosis inhibitor but also elucidate its mechanism of action via direct binding and Nrf2 pathway activation,providing a promising therapeutic candidate for ischemic stroke. 展开更多
关键词 Ferroptosis Ischemic stroke Tamarixetin Neuron Nuclear factor erythroid-2-related factor 2
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Long-term real-world PM2.5 exposure induces depression-like behaviors in mice by disrupting nuclear factor erythroid 2-related factor 2-mediated astrocyte-to-microglia communication 认领 引用
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作者 Nannan Huang Weiqing Shi +4 位作者 Cuishuang Dong Bin Li Yaohan Wang Hanqing Chen Xiaobo Li 《Neural Regeneration Research》 SCIE CAS CSCD 2026年第7期3238-3248,共11页
Long-term exposure to ambient fine particulate matter(PM2.5)may increase the risk of neurotoxicity in human populations.However,research studies on the underlying mechanisms of chronic PM2.5-induced depression-like be... Long-term exposure to ambient fine particulate matter(PM2.5)may increase the risk of neurotoxicity in human populations.However,research studies on the underlying mechanisms of chronic PM2.5-induced depression-like behaviors,and potential therapeutical strategies,remain scarce.In the present study,after long-term exposure to real-world PM2.5 for 15 weeks,male mice displayed depression-like behaviors,which were revealed using the open field and sucrose preference tests.Mechanistically,chronic PM2.5 exposure promoted astrocytic A1 polarization and disrupted reduction-oxidation balance in the mouse hippocampus.Furthermore,PM2.5-exposed mice displayed pathological damage to hippocampal neurons as well as the inhibition of nuclear factor erythroid 2-related factor 2 signaling.Astrocytic ablation of nuclear factor erythroid 2-related factor 2 exacerbated PM2.5-induced hippocampal neuronal injury in mice via the disruption of astrocyte-to-microglia communication;this finding was confirmed in mice with bilateral and unilateral hippocampal astrocytic Nfe2l2 knockdown.Importantly,the upregulation of nuclear factor erythroid 2-related factor 2 activation by procyanidin significantly ameliorated PM2.5-induced depression-like behaviors through the remodeling of astrocyte-to-microglia communication.Together,our findings shed light on the important role of hippocampal astrocytic nuclear factor erythroid 2-related factor 2 activation for maintaining astrocyte-to-microglia communication,and indicate potential research avenues for therapeutic strategies against PM2.5-induced depresson-like behaviors. 展开更多
关键词 air pollution astrocyte-to-microglia communication depression-like behaviors fine particulate matter(PM2.5) neurotoxicity nuclear factor erythroid 2-related factor 2 oxidative stress procyanidins
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Rhapontin activating nuclear factor erythroid 2-related factor 2 to ameliorate Parkinson’s disease-associated gastrointestinal dysfunction 认领 引用
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作者 Yi-Xiao Chen Na-Qi Sun Sai-Jun Mo 《World Journal of Gastroenterology》 SCIE CAS 2026年第4期121-125,共5页
This commentary provides a critical evaluation of the study by Wang et al,which focuses on rhapontin activating colonic nuclear factor erythroid 2-related factor 2(NRF2)to explore its therapeutic potential for Parkin... This commentary provides a critical evaluation of the study by Wang et al,which focuses on rhapontin activating colonic nuclear factor erythroid 2-related factor 2(NRF2)to explore its therapeutic potential for Parkinson’s disease(PD)-associated gastrointestinal dysfunction.The commentary acknowledges the academic value of the study:It has not only validated intestinal NRF2 as a therapeutic target for PD but also provided experimental support for the“enteric pathology hypothesis”.However,several key gaps remain unresolved in the study.At the gut microbiota level,the exploration of the causal relationship of the microbiota is insufficient,with no validation conducted via methods such as fecal microbiota transplantation;additionally,it fails to systematically integrate the gut-brain axis with PD and does not assess the impact of rhapontin on the composition or function of the gut microbiota.At the pathway mechanism level,it lacks an analysis of the crosstalk between NRF2 and other rhapontin-targeted pathways,including nuclear factor kappa-B,mitogen-activated protein kinase,adenosine monophosphate-activated protein kinase,and sirtuin 1.At the experimental method level,the behavioral testing methods for PD mouse models and the limitations of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced mouse models need attention.Additionally,certain flaws exist in some experimental result figures.Furthermore,this commentary puts forward improvement suggestions for the study.Future research should prioritize multi-omics analysis,encompassing combined metabolomics and metagenomics detection,while conducting mechanistic validation of NRF2-interacting molecules(KEAP1 and p62).In addition,it is necessary to improve refined behavioral tests,focusing on incorporating cognitive function and anxiety-related assessment items. 展开更多
关键词 Rhapontin Gastrointestinal dysfunction Parkinson’s disease Nuclear factor erythroid 2-related factor 2 Antiinflammatory
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Activation of the nucleus nuclear factor erythroid 2-related factor 2 via ghrelin/growth hormone secretagogue receptor 1a signaling by Yueju pill(越鞠丸)confers cardioprotective and antidepressant effects 认领 引用
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作者 JING Yunjia YE Zhaoyi +6 位作者 ZHU Yan GAO Xin CHEN Xi WANG Kaixuan HUANG Dafeng HU Yue JIANG Jiancong 《Journal of Traditional Chinese Medicine》 SCIE CAS CSCD 2026年第3期517-529,共13页
OBJECTIVE:To investigate the efficacy and mechanistic foundations of the Traditional Chinese Medicine Yueju pill(YJP,越鞠丸)for treating the complex comorbidity of heart failure and depression.METHODS:C57BL/6 male mic... OBJECTIVE:To investigate the efficacy and mechanistic foundations of the Traditional Chinese Medicine Yueju pill(YJP,越鞠丸)for treating the complex comorbidity of heart failure and depression.METHODS:C57BL/6 male mice were used to establish a robust congestive heart failure(CHF)model with concomitant depressive manifestations.Echocardiographic assessments were conducted to evaluate cardiac structure and function in the mice.Depression-related behavioral tests and the detection of monoamine neurotransmitters were performed to assess the antidepressant-like effectiveness of YJP.Western blot analysis was conducted to measure the expression levels of key components in the nuclear factor erythroid 2-related factor 2(NRF2)/heme oxygenase 1(HO1)antioxidant pathway,NRF2/brain-derived neurotrophic factor(BDNF)pathway,and ghrelin/growth hormone secretagogue receptor(GHS-R)1a pathway in the myocardium and hippocampus.To explore the mechanistic role of the ghrelin/GHS-R1a pathway,the ghrelin receptor antagonist D-Lys3-growth hormone releasing peptide-6 was introduced to enable the iterative evaluation of the aforementioned parameters.RESULTS:YJP improved cardiac dysfunction and myocardial fibrosis and markedly ameliorated depressive behaviors.It also improved neuron damage,boosted the growth of dendritic spines to enhance synaptic plasticity,and alleviated monoamine neurotransmitter imbalances.Additionally,the NRF2/BDNF,ghrelin/GHS-R1a,and NRF2/HO1 antioxidant pathways were promoted by YJP,with the increased expression of key components of the three pathways.The addition of a GHS-R1a antagonist impaired the antidepressant and cardioprotective effects of YJP.CONCLUSIONS:YJP effectively improved cardiac dysfunction and depressive-like behaviors in mice by activating NRF2 via mediation of the ghrelin/GHS-R1a signaling axis within both the myocardial and hippocampal domains. 展开更多
关键词 depression heart failure NF-E2-related factor 2 ghrelin receptors ghrelin Yueju pill
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Zhongfeng Xingnao Liquid ameliorates post-stroke cognitive impairment through sirtuin1(SIRT1)/nuclear factor erythroid 2-related factor 2(Nrf2)/heme oxygenase 1(HO-1)pathway 认领 引用 被引量：5
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作者 Wenqin Yang Wen Wen +4 位作者 Hao Chen Haijun Zhang Yun Lu Ping Wang Shijun Xu 《Chinese Journal of Natural Medicines》 SCIE CAS CSCD 2025年第1期77-89,共13页
The activation of the sirtuin1(SIRT1)uclear factor erythroid 2-related factor 2(Nrf2)/heme oxygenase 1(HO-1)pathway has been shown to mitigate oxidative stress-induced apoptosis and mitochondrial damage by reducing re... The activation of the sirtuin1(SIRT1)uclear factor erythroid 2-related factor 2(Nrf2)/heme oxygenase 1(HO-1)pathway has been shown to mitigate oxidative stress-induced apoptosis and mitochondrial damage by reducing reactive oxygen species(ROS)levels.Clinical trials have demonstrated that Zhongfeng Xingnao Liquid(ZFXN)ameliorates post-stroke cognitive impairment(PSCI).However,the underlying mechanism,particularly whether it involves protecting mitochondria and inhibiting apoptosis through the SIRT1/Nrf2/HO-1 pathway,remains unclear.This study employed an oxygen-glucose deprivation(OGD)cell model using SHSY5Y cells and induced PSCI in rats through modified bilateral carotid artery ligation(2VO).The effects of ZFXN on learning and memory,neuroprotective activity,mitochondrial function,oxidative stress,and the SIRT1/Nrf2/HO-1 pathway were evaluated both in vivo and in vitro.Results indicated that ZFXN significantly increased the B-cell lymphoma 2(Bcl2)/Bcl2-associated X(Bax)ratio,reduced terminal deoxynucleotidyl transferase-mediated d UTP nickend-labeling(TUNEL)+cells,and markedly improved cognition,synaptic plasticity,and neuronal function in the hippocampus and cortex.Furthermore,ZFXN exhibited potent antioxidant activity,evidenced by decreased ROS and malondialdehyde(MDA)content and increased superoxide dismutase(SOD),catalase(CAT),and glutathione(GSH)levels.ZFXN also demonstrated considerable enhancement of mitochondrial membrane potential(MMP),Tom 20 fluorescence intensity,adenosine triphosphate(ATP)and energy charge(EC)levels,and mitochondrial complexⅠandⅢactivity,thereby inhibiting mitochondrial damage.Additionally,ZFXN significantly increased SIRT1 activity and elevated SIRT1,nuclear Nrf2,and HO-1 levels.Notably,these effects were substantially counteracted when SIRT1 was suppressed by the inhibitor EX-527 in vitro.In conclusion,ZFXN alleviates PSCI by activating the SIRT1/Nrf2/HO-1 pathway and preventing mitochondrial damage. 展开更多
关键词 Zhongfeng Xingnao Liquid Post-stroke cognitive impairment Oxidative stress Mitochondrial function Apoptosis Sirtuin1uclear factor erythroid 2-related factor 2/heme oxygenase 1 pathway
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Nuclear Dbf2-related Kinase 1 functions as tumor suppressor in glioblastoma by phosphorylation of Yes-associated protein 认领 引用
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作者 Bin Chen Bin Liu +3 位作者 Tao Yu Yun-Feng Han Chao Wu Zhen-Yu Wang 《Chinese Medical Journal》 SCIE CAS CSCD 2021年第17期2054-2065,共12页
Background:The Nuclear Dbf2-related(NDR1)kinase is a member of the NDR/LATS family,which was a supplementary of Hippo pathway.However,whether NDR1 could inhibit glioblastoma(GBM)growth by phosphorylating Yes-associate... Background:The Nuclear Dbf2-related(NDR1)kinase is a member of the NDR/LATS family,which was a supplementary of Hippo pathway.However,whether NDR1 could inhibit glioblastoma(GBM)growth by phosphorylating Yes-associated protein(YAP)remains unknown.Meanwhile,the role of NDR1 in GBM was not clear.This study aimed to investigate the role of NDR1-YAP pathway in GBM.Methods:Bioinformation analysis and immunohistochemistry(IHC)were performed to identify the expression of NDR1 in GBM.The effect of NDR1 on cell proliferation and cell cycle was analyzed utilizing CCK-8,clone formation,immunofluorescence and flow cytometry,respectively.In addition,the xenograft tumor model was established as well.Protein interaction was examined by Coimmunoprecipitation and immunofluorescence to observe co-localization.Results:Bioinformation analysis and IHC of our patients’tumor tissues showed that expression of NDR1 in tumor tissue was relatively lower than that in normal tissues and was positively related to a lower survival rate.NDR1 could markedly reduce the proliferation and colony formation of U87 and U251.Furthermore,the results of flow cytometry showed that NDR1 led to cell cycle arrest at the G1 phase.Tumor growth was also inhibited in xenograft nude mouse models in NDR1-overexpression group.Western blotting and immunofluorescence showed that NDR1 could integrate with and phosphorylate YAP at S127 site.Meanwhile,NDR1 could mediate apoptosis process.Conclusion:In summary,our findings point out that NDR1 functions as a tumor suppressor in GBM.NDR1 is identified as a novel regulator of YAP,which gives us an in-depth comprehension of the Hippo signaling pathway. 展开更多
关键词 Glioblastoma Hippo signaling pathway Nuclear Dbf2-related Yes-associated protein
Modulating nuclear factor erythroid 2-related factor 2 and heme oxygenase-1 in liver-brain axis disorders 认领 引用 被引量：1
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作者 Yi-Ming Zhang Zhi-Gang Zhang 《World Journal of Psychiatry》 SCIE 2025年第9期57-78,共22页
A broad spectrum of liver disorders and their associated complications most notably hepatic encephalopathy impact millions of individuals worldwide,including conditions such as non-alcoholic fatty liver disease,alcoho... A broad spectrum of liver disorders and their associated complications most notably hepatic encephalopathy impact millions of individuals worldwide,including conditions such as non-alcoholic fatty liver disease,alcoholic liver injury,viral hepatitis,hepatic fibrosis,cirrhosis,and hepatocellular carcinoma.The underlying pathogenic mechanisms are multifactorial,encompassing oxidative stress,inflammatory cascades,mitochondrial impairment,and disturbances in immune homeostasis.Hepatic encephalopathy patients experience cognitive impairment,mood disturbances,and psychomotor dysfunction,significantly reducing quality of life through mechanisms including oxidative stress,neuroinflammation,and neurotransmitter imbalances.The nuclear factor erythroid 2-related factor 2(Nrf2)/heme oxygenase-1(HO-1)signaling pathway serves as a critical antioxidative defense mechanism in these conditions.Nrf2 regulates the expression of protective enzymes,while HO-1 exerts anti-inflammatory,anti-apoptotic,and antifibrotic effects through heme degradation products.Natural herbal monomers as Nrf2 activators offer advantages of low toxicity,multi-target actions,and extensive traditional use.Various herbal monomers demonstrate specific effects against different liver diseases:In fatty liver,baicalin alleviates lipid accumulation and inflammation;In alcoholic liver disease,curcumin enhances Nrf2 activity reducing oxidative damage;In drug-induced liver injury,dihydromyricetin mitigates oxidative stress;In viral hepatitis,andrographolide inhibits hepatitis C virus replication;In liver fibrosis,multiple compounds inhibit stellate cell activation.These natural compounds simultaneously alleviate hepatic dysfunction and neuropsychiatric symptoms by modulating the Nrf2/HO-1 pathway,though clinical application still faces challenges such as low bioavailability,requiring further research. 展开更多
关键词 Nuclear factor erythroid 2-related factor 2/heme oxygenase-1 pathway Liver brain axis dysfunction Hepatic encephalopathy Cognitive impairment Depression Anxiety
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Effect of fish scale ointment on diabetic foot ulcer by inducing ferroptosis via the nuclear factor E2-related factor 2 pathway 认领 引用
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作者 Lin Li Xiao-Na Liu +4 位作者 Shuang Guo Yan-Ling Ju Lan-Yue Guo Chun-Hua Zhang Jin-Jun Wang 《World Journal of Diabetes》 SCIE 2025年第12期137-147,共11页
BACKGROUND Excessive oxidative stress plays a key role in the development of diabetic complications,including impaired ulcer healing.Previous studies have shown that fish scale ointment can promote wound healing.AIM T... BACKGROUND Excessive oxidative stress plays a key role in the development of diabetic complications,including impaired ulcer healing.Previous studies have shown that fish scale ointment can promote wound healing.AIM To preliminarily investigate the effect of fish scale ointment on wound healing in a diabetic foot ulcer(DFU)rat model by examining its regulation of the nuclear factor E2-related factor 2(Nrf2)pathway and induction of ferroptosis.METHODS Fish scale ointment(collagen product)was prepared from 500 g of silver carp scales.A diabetic rat model was induced by high-fat and high-sugar feeding combined with intraperitoneal streptozotocin injections.For the DFU rat model,ulcer wounds were created by removing dorsal foot hair and cutting the skin to the fascia.The diabetic rats were randomized into five groups:Model,fish scale collagen(FSC),control+liproxstatin-1(Lip-1),model+Lip-1,and FSC+Lip-1.In each group,treatments were administered once daily by topical application and intraperitoneal injection for 14 days.Wound healing was evaluated on days 7 and 14 after treatment.Hematoxylin and eosin staining was used to assess wound injury and capillary formation.Basic fibroblast growth factor(bFGF)and CD31 levels in wound tissue were measured by immunohistochemistry.Additionally,malondialdehyde(MDA),glutathione(GSH),ferroptosis-associated genes,and iron ion concentrations were quantified using assay kits.Protein levels of Nrf2,heme oxygenase-1(HO-1),and glutathione peroxidase 4(GPX4)were determined using Western blotting.RESULTS Compared with the control group,the model group showed slower wound healing,reduced angiogenesis,decreased bFGF and CD31 levels,increased iron ion concentration and MDA levels,reduced GSH levels,and decreased Nrf2,HO-1,and GPX4 protein expression(all P<0.05).The FSC,model+Lip-1,and FSC+Lip-1 groups showed increased wound healing and angiogenesis,elevated bFGF and CD31 expression,lowered iron ion concentration and MDA levels,increased GSH levels,and enhanced Nrf2,HO-1,and GPX4 protein levels compared with the model group(P<0.05).Improvements were more pronounced in the FSC+Lip-1 group compared with the FSC group(P<0.05).CONCLUSION Fish scale ointment promotes angiogenesis and wound healing in DFU rat models by inhibiting ferroptosis,possibly through the activation of the Nrf2 pathway. 展开更多
关键词 Fish scale ointment Nuclear factor E2-related factor 2 pathway Ferroptosis Diabetic foot ulcer Fish scale collagen
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Rhapontin activates nuclear factor erythroid 2-related factor 2 to ameliorate 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced gastrointestinal dysfunction in Parkinson's disease mice 认领 引用 被引量：1
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作者 Xin-Yu Wang Fang Liu +4 位作者 Qi-Tong Wang Shu-Zhu Li Yu-Zhao Ye Tao Chen Ben-Chi Cai 《World Journal of Gastroenterology》 SCIE CAS 2025年第15期96-108,共13页
BACKGROUND Parkinson's disease(PD)-a progressive neurodegenerative disorder-is characterized by motor and gastrointestinal dysfunction.The exploration of novel therapeutic strategies for PD is vital.AIM To investi... BACKGROUND Parkinson's disease(PD)-a progressive neurodegenerative disorder-is characterized by motor and gastrointestinal dysfunction.The exploration of novel therapeutic strategies for PD is vital.AIM To investigate the potential mechanism of action of rhapontin-a natural compound with known antioxidant and anti-inflammatory properties-in the context of PD.METHODS Network pharmacology was used to predict the targets and mechanisms of action of rhapontin in PD.Behavioral tests and tyrosine hydroxylase immunofluorescence analysis were used to assess the effect of rhapontin on symptoms and pathology in MPTP-induced mice.Interleukin(IL)-6,IL-1β,tumor necrosis factor(TNF)-α,and IL-10 levels in tissues were measured using an enzyme-linked immunosorbent assay(ELISA).Additionally,nuclear factor erythroid 2-related factor 2(NRF2)activation was confirmed using western blotting.RESULTS NRF2 was predicted to be the key transcription factor underlying the therapeutic effects of rhapontin in PD,and its anti-PD action may be associated with its antiinflammatory and antioxidant properties.Rhapontin ameliorated the loss of dopaminergic neurons and gastrointestinal dysfunction in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine(MPTP)-induced mice by activating NRF2.Additio-nally,rhapontin treatment significantly decreased pro-inflammatory cytokines(IL-6,TNF-α,IL-1β)in the substantia nigra,striatum,and colon,whereas it increased anti-inflammatory cytokine(IL-10)levels only in the colon,indicating the involvement of gut–brain axis in its neuroprotective potential.Finally,NRF2 was identified as a key transcription factor activated by rhapontin,particularly in the colon.CONCLUSION We elucidated the effects of rhapontin in MPTP-induced PD mouse models using a combination of network pharmacology analysis,behavioral assessments,immunofluorescence,ELISA,and Western blotting.Our findings revealed the multifaceted role of rhapontin in ameliorating PD through its anti-inflammatory and antioxidant properties,particularly by activating NRF2,paving the way for future research into targeted therapies for PD. 展开更多
关键词 Rhapontin Gastrointestinal dysfunction Parkinson’s disease Nuclear factor erythroid 2-related factor 2 Gut-Brain axis Oxidative stress Neuroinflammation
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Targeting sirtuin 1/nuclear factor erythroid 2-related factor 2/tumor necrosis factor-αpathway to modulate hepatic ischemia reperfusioninduced injury 认领 引用
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作者 Mina Thabet Kelleni Walaa Yehia Abdelzaher +3 位作者 Marly Adly Mina Ezzat Attya Michael A Fawzy Mohamed Abdellah Ibrahim 《World Journal of Hepatology》 2025年第12期184-195,共12页
BACKGROUND Hepatic ischemia reperfusion(HIR)injury is a major complication affecting various major liver surgeries,including liver transplantation.Aprepitant(APRE),a neurokinin-1 receptor antagonist,is commonly used a... BACKGROUND Hepatic ischemia reperfusion(HIR)injury is a major complication affecting various major liver surgeries,including liver transplantation.Aprepitant(APRE),a neurokinin-1 receptor antagonist,is commonly used as an antiemetic to prevent chemotherapy-induced nausea and vomiting.AIM To assess the potential protective effect of APRE against HIR-induced liver injury via targeting the nucleotide-binding oligomerization domain-,leucine-rich repeat-,and pyrin domain-containing receptor 3/interleukin(IL)-1beta signaling pathway.METHODS Six groups of adult male Wistar albino rats were divided as follows:Sham group,Sham/APRE10 group(APRE 10 mg/kg),HIR group,HIR/APRE5 group(APRE 5 mg/kg),HIR/APRE10 group(APRE 10 mg/kg),and HIR/APRE20 group(APRE 20 mg/kg).Serum alanine transaminase,aspartate transaminase,liver malondialdehyde,total antioxidant capacity levels,as well as IL-6,sirtuin 1(Sirt1),caspase-3,cleaved caspase-3,and tumor necrosis factor alpha biomarkers,were evaluated.Hepatic specimens were examined histopathologically and immunohistochemically for nuclear factor erythroid-2-related factor 2(Nrf2)immunoexpression.RESULTS HIR resulted in hepatic damage,as evidenced by histopathological changes and a significant increase in serum alanine transaminase,aspartate transaminase,hepatic malondialdehyde,caspase-3,and tumor necrosis factor alpha levels.Additionally,there were significant increases in hepatic total antioxidant capacity and reductions in IL-6 and cleaved caspase-3 protein levels,as demonstrated by Western blot analysis,along with enhanced immunoexpression of Sirt1 and Nrf2.APRE has significantly reduced various parameters of oxidative stress,inflammation,and apoptosis,and a significant increase in liver Nrf2 immunoexpression,leading to a significant improvement in the histopathological changes.CONCLUSION In conclusion,targeting the Sirt1/Nrf2 signaling pathway,as demonstrated by APRE in our model,could present a promising therapeutic target to protect against HIR-induced liver injury during major liver surgeries. 展开更多
关键词 Hepatic ischemia reperfusion injury Aprepitant Sirtuin 1 Nuclear factor erythroid-2-related factor 2 Tumor necrosis factor alpha
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Erianin mitigates diabetic cardiomyopathy via adenosine monophosphate-activated protein kinase-nuclear factor erythroid 2-related factor 2-heme oxygenase-1 pathway activation 认领 引用 被引量：1
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作者 Jia-Hui Chen Xiao-Chun Dai +1 位作者 Zi-Jiao Quan Xin-Yu Liu 《World Journal of Diabetes》 SCIE 2025年第6期279-293,共15页
BACKGROUND Erianin is a natural bibenzyl compound extracted from Dendrobium chrysotoxum and is known for its anti-inflammatory and antioxidant properties.AIM To explore the possible therapeutic mechanisms of erianin a... BACKGROUND Erianin is a natural bibenzyl compound extracted from Dendrobium chrysotoxum and is known for its anti-inflammatory and antioxidant properties.AIM To explore the possible therapeutic mechanisms of erianin and determine if it can reduce cardiac damage in mice with type 2 diabetes.METHODS High-fat diet and intraperitoneal injections of streptozotocin were used to induce type 2 diabetes mellitus in C57BL/6 mice.Mice were divided into different groups including control,model,and treatment with various doses of erianin(10,20,and 40 mg/kg)as well as ML-385+erianin group.RESULTS Erianin reduced oxidative stress and inflammation and alleviated diabetic cardiomyopathy through the activation of the adenosine monophosphate-acti-vated protein kinase(AMPK)-nuclear factor erythroid 2-related factor 2(Nrf2)-heme oxygenase-1(HO-1)pathway.Treatments with erianin-M and erianin-H promoted weight stabilization and normalized fasting glucose levels relative to diabetic controls.Echocardiographic assessment demonstrated that erianin dose-dependently enhanced left ventricular systolic function(left ventricular ejection fraction,left ventricular fractional shortening)and mitigated ventricular remodeling(left ventricular internal diameter at end-diastole,left ventricular internal diameter at end-systole;P<0.05 vs model group).No significant differences were observed between the ML-385+erianin and placebo-treated groups.Histopathological examination through hematoxylin-eosin staining indicated that erianin ameliorated myocardial fiber fragmentation,structural disorganization,inflammatory cell infiltration,and cytolytic damage.Furthermore,it significantly reduced the serum levels of cardiac troponin I,creatine kinase,and its MB isoenzyme.However,the ML-385+erianin co-treatment failed to alleviate myocardial injury.Metabolic profiling revealed erianin-mediated improvements in glycemic regulation(glycated hemoglobin:P<0.001),plasma insulin homeostasis,and lipid metabolism(total cholesterol,triglycerides,low-density lipo-protein cholesterol reduction,and high-density lipoprotein cholesterol restoration;P<0.05 vs model group).Pro-inflammatory cytokines including tumor necrosis factor-α,interleukin(IL)-1β,and IL-6 were markedly suppressed in the erianin-M and erianin-H groups compared with the model group,whereas no significant differences were detected between the model and ML-385+erianin groups.Oxidative stress parameters showed decreased malondialdehyde levels accompanied by elevated superoxide dismutase and catalase activities in erianin-treated groups,with the most pronounced effects in the erianin-H group(P<0.05).Western blot analysis confirmed the significant upregulation of proteins associated with the AMPK/Nrf2/HO-1 pathway in erianin-M and erianin-H groups.These protective effects were abolished in the ML-385+erianin co-treatment group,which showed no statistical differences from the model group.CONCLUSION Erianin can effectively alleviate myocardial injury in type 2 diabetic mice by activating the AMPK-Nrf2-HO-1 pathway. 展开更多
关键词 Erianin Diabetic cardiomyopathy Adenosine monophosphate-activated protein kinase pathway Nuclear factor erythroid 2-related factor 2 Cardioprotection Oxidative stress
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Role of nuclear factor erythroid 2-related factor 2 in negative pressure wound therapy for diabetic foot ulcers 认领 引用 被引量：1
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作者 Hao-Jie Sun Shan-Wen Si +3 位作者 Ya-Mei Ma Xue-Kui Liu Hou-Fa Geng Jun Liang 《World Journal of Diabetes》 SCIE 2025年第5期363-373,共11页
BACKGROUND Negative pressure wound therapy(NPWT)is a potential treatment for diabetic foot ulcers(DFUs),although the mechanisms underlying its effectiveness remain unclear.This study posits that NPWT may improve wound... BACKGROUND Negative pressure wound therapy(NPWT)is a potential treatment for diabetic foot ulcers(DFUs),although the mechanisms underlying its effectiveness remain unclear.This study posits that NPWT may improve wound healing by promoting angiogenesis and activating the nuclear factor erythroid 2-related factor 2(Nrf2)/Kelch-like epichlorohydrin-associated protein 1(Keap1)signaling pathway,which is crucial for the body’s defense against oxidative stress.The hypothesis indicates that enhancing antioxidant defenses through NPWT may positively affect the healing process.There are still limited data on the roles of Nrf2,its downstream signaling molecules,and angiogenesis markers in patients undergoing NPWT.AIM To study the mechanism of NPWT in DFUs.METHODS This study included a total of 40 hospitalized patients with DFUs from Xuzhou Central Hospital,who were divided into Control group(n=21)and NPWT group(n=19).The levels of Nrf2 and Keap1 were analyzed in the granulation tissue 7 days after treatment.The wound condition,erythrocyte sedimentation rate(ESR),procalcitonin(PCT),interleukin 6(IL-6),tumor necrosis factor alpha(TNF-α),vascular endothelial growth factor(VEGF),basic fibroblast growth factor(b-FGF),cluster of differentiation 31(CD31),and levels of oxidative stress[malondialdehyde(MDA),superoxide dismutase(SOD),catalase(CAT),and total antioxidant capacity(T-AOC)]were analyzed before and 7 days after treatment by the Mann-Whitney U test.RESULTS The NPWT group demonstrated significant improvements in wound healing compared to the control group after 7 days of treatment.The levels of ESR,PCT,IL-6,and TNF-αwere significantly reduced in the NPWT group compared to the control group(P<0.05),while the levels of CD31,VEGF,and b-FGF showed significant increases(P<0.05).The NPWT group exhibited notable elevations in the levels of Nrf2 and its downstream targets(SOD,CAT,and T-AOC),accompanied by decreases in the levels of Keap1 and MDA(P<0.05).CONCLUSION NPWT may contribute to the healing of DFUs by potentially reducing levels of oxidative stress.Its effects could possibly be enhanced through the action of Nrf2. 展开更多
关键词 Negative pressure wound therapy Diabetic foot ulcers Nuclear factor erythroid 2-related factor 2 Kelch-like epichlorohydrin-associated protein 1 Healing
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Neuroprotective effects of salidroside on focal cerebral ischemia/reperfusion injury involve the nuclear erythroid 2-related factor 2 pathway 认领 引用 被引量：29
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作者 Jing Han Qing Xiao +4 位作者 Yan-hua Lin Zhen-zhu Zheng Zhao-dong He Juan Hu Li-dian Chen 《Neural Regeneration Research》 SCIE CAS CSCD 2015年第12期1989-1996,共8页
Salidroside,the main active ingredient extracted from Rhodiola crenulata,has been shown to be neuroprotective in ischemic cerebral injury,but the underlying mechanism for this neuroprotection is poorly understood.In t... Salidroside,the main active ingredient extracted from Rhodiola crenulata,has been shown to be neuroprotective in ischemic cerebral injury,but the underlying mechanism for this neuroprotection is poorly understood.In the current study,the neuroprotective effect of salidroside on cerebral ischemia-induced oxidative stress and the role of the nuclear factor erythroid 2-related factor 2（Nrf2）pathway was investigated in a rat model of middle cerebral artery occlusion.Salidroside（30 mg/kg）reduced infarct size,improved neurological function and histological changes,increased activity of superoxide dismutase and glutathione-S-transferase,and reduced malon-dialdehyde levels after cerebral ischemia and reperfusion.Furthermore,salidroside apparently increased Nrf2 and heme oxygenase-1 expression.These results suggest that salidroside exerts its neuroprotective effect against cerebral ischemia through anti-oxidant mechanisms and that activation of the Nrf2 pathway is involved.The Nrf2/antioxidant response element pathway may become a new therapeutic target for the treatment of ischemic stroke. 展开更多
关键词 nerve regeneration traditional Chinese medicine salidroside cerebral ischemia andreperfusion nuclear factor erythroid 2-related factor 2 heme oxygenase-1 middle cerebral arteryocclusion model superoxide dismutase neuroprotection neural regeneration
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Neferine inhibits the progression of diabetic nephropathy by modulating the miR-17-5p/nuclear factor E2-related factor 2 axis 认领 引用 被引量：9
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作者 HUANG Hongmei YANG Maojun +6 位作者 LI Ting WANG Dandan LI Ying TANG Xiaochi YUAN Lu GU Shi XU Yong 《Journal of Traditional Chinese Medicine》 SCIE CSCD 2024年第1期44-53,共10页
OBJECTIVE:To investigate the effect of Neferine(Nef)on diabetic nephropathy(DN)and to explore the mechanism of Nef in DN based on miRNA regulation theory.METHODS:A DN mouse model was constructed and treated with Nef.S... OBJECTIVE:To investigate the effect of Neferine(Nef)on diabetic nephropathy(DN)and to explore the mechanism of Nef in DN based on miRNA regulation theory.METHODS:A DN mouse model was constructed and treated with Nef.Serum creatinine(Crea),blood urea(UREA)and urinary albumin were measured in mice by kits,and renal histopathological changes and fibrosis were observed by hematoxylin-eosin staining and Masson staining.Renal tissue superoxide dismutase(SOD),malondialdehyde(MDA)and glutathione peroxidase(GSH-Px)activities were measured by enzyme-linked immunosorbent assay(ELISA).Western blotting was used to detect the expression of nuclear factor E2-related factor 2(Nrf2)/heme oxygenase 1(HO-1)signaling pathway-related proteins in kidney tissues.Quantitative reverse transcription-polymerase chain reaction(q RT-PCR)was used to detect the expression of miR-17-5p in kidney tissues.Subsequently,a DN in vitro model was constructed by high glucose culture of human mesangial cells(HMCs),cells were transfected with miR-17-5p mimic and/or treated with Nef,and we used q RTPCR to detect cellular miR-17 expression,flow cytometry to detect apoptosis,ELISAs to detect cellular SOD,MDA,and GSH-Px activities,Western blots to detect Nrf2/HO-1 signaling pathway-related protein expression,and dual luciferase reporter gene assays to verify the targeting relationship between Nrf2 and miR-17-5p.RESULTS:Administration of Nef significantly reduced the levels of blood glucose,Crea,and UREA and the expression of miR-17-5p,improved renal histopathology and fibrosis,significantly reduced MDA levels,elevated SOD and GSH-Px activities,and activated Nrf2 expression in kidney tissues from mice with DN.Nrf2 is a post-transcriptional target of miR-17-5p.In HMCs transfected with miR-17-5p mimics,the m RNA and protein levels of Nrf2 were significantly suppressed.Furthermore,miR-17-5p overexpression and Nef intervention resulted in a significant increase in high glucose-induced apoptosis and MDA levels in HMCs and a significant decrease in the protein expression of HO-1 and Nrf2.CONCLUSION:Collectively,these results indicate that Nef has an ameliorative effect on DN,and the mechanism may be through the miR-17-5p/Nrf2 pathway. 展开更多
关键词 diabetic nephropathies neferine miR-17-5p NF-E2-related factor 2 oxidative stress
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Interplay between nuclear factor erythroid 2-related factor 2 and inflammatory mediators in COVID-19-related liver injury 认领 引用 被引量：4
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作者 Dan-Dan Zhu Xue-Mei Tan +9 位作者 Li-Qing Lu Si-Jia Yu Ru-Li Jian Xin-Fang Liang Yi-Xuan Liao Wei Fan LucíiaBarbier-Torres Austin Yang He-Ping Yang Ting Liu 《World Journal of Gastroenterology》 SCIE CAS 2021年第22期2944-2962,共19页
Coronavirus disease 2019(COVID-19)caused by severe acute respiratory syndrome coronavirus 2 is a global pandemic and poses a major threat to human health worldwide.In addition to respiratory symptoms,COVID-19 is usual... Coronavirus disease 2019(COVID-19)caused by severe acute respiratory syndrome coronavirus 2 is a global pandemic and poses a major threat to human health worldwide.In addition to respiratory symptoms,COVID-19 is usually accompanied by systemic inflammation and liver damage in moderate and severe cases.Nuclear factor erythroid 2-related factor 2(NRF2)is a transcription factor that regulates the expression of antioxidant proteins,participating in COVID-19-mediated inflammation and liver injury.Here,we show the novel reciprocal regulation between NRF2 and inflammatory mediators associated with COVID-19-related liver injury.Additionally,we describe some mechanisms and treatment strategies. 展开更多
关键词 COVID-19-related liver injury Nuclear factor erythroid 2-related factor 2 Inflammatory mediator Oxidative stress Therapeutic targets
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Liver expression of Nrf2-related genes in different liver diseases 认领 引用 被引量：10
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作者 Ming-Liang Cheng Yuan-Fu Lu +2 位作者 Hong Chen Zhong-Yang Shen Jie Liu 《Hepatobiliary & Pancreatic Diseases International》 SCIE CAS CSCD 2015年第5期485-491,共7页
BACKGROUND： The KEAP1-Nrf2 antioxidant signaling pathway is important in protecting liver from various insults. However,little is known about the expression of Nrf2-related genes in human liver in different diseases.... BACKGROUND： The KEAP1-Nrf2 antioxidant signaling pathway is important in protecting liver from various insults. However,little is known about the expression of Nrf2-related genes in human liver in different diseases.METHODS： This study utilized normal donor liver tissues（n=35）, samples from patients with hepatocellular carcinoma（HCC, n=24）, HBV-related cirrhosis（n=27）, alcoholic cirrhosis（n=5） and end-stage liver disease（n=13）. All of the liver tissues were from the Oriental Liver Transplant Center, Beijing,China. The expressions of Nrf2 and Nrf2-related genes, including its negative regulator Kelch-like ECH-associated protein 1（KEAP1）, its targeted gene NAD（P）H-quinone oxidoreductase 1（NQO1）, glutamate-cysteine ligase catalytic subunit（GCLC） and modified subunit（GCLM）, heme oxygenase 1（HO-1） and peroxiredoxin-1（PRDX1） were evaluated. RESULTS： The expression of Nrf2 was decreased in HCC, increased in alcoholic cirrhosis and end-stage liver disease. The expression of KEAP1 was increased in all of the liver samples.The most notable finding was the increased expression of NQO1 in HCC（18-fold）, alcoholic cirrhosis（6-fold）, endstage liver disease（5-fold） and HBV-related cirrhosis（3-fold）.Peri-HCC also had 4-fold higher NQO1 m RNA as compared to the normal livers. GCLC m RNA levels were lower only in HCC, as compared to the normal livers and peri-HCC tissues.GCLM m RNA levels were higher in HBV-related cirrhosis and end-stage liver disease. HO-1 m RNA levels were increased in all liver tissues except for HCC. Peri-HCC had higher PRDX1 m RNA levels compared with HCC and normal livers.CONCLUSION： Nrf2 and Nrf2-related genes are aberrantly expressed in the liver in different diseases and the increase of NQO1 was the most notable finding, especially in HCC. 展开更多
关键词 Nrf2-related gene expression cirrhosis hepatocellular carcinoma end-stage liver disease
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Emerging trends and hotspots of Nuclear factor erythroid 2-related factor 2 in nervous system diseases 认领 引用 被引量：1
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作者 Xue-Qin Chang Ling Xu +3 位作者 Yi-Xuan Zuo Yi-Guo Liu Jia Li Hai-Tao Chi 《World Journal of Clinical Cases》 SCIE 2023年第32期7833-7851,共19页
BACKGROUND The Nuclear factor erythroid 2-related factor 2(NRF2)transcription factor has attracted much attention in the context of neurological diseases.However,none of the studies have systematically clarified this ... BACKGROUND The Nuclear factor erythroid 2-related factor 2(NRF2)transcription factor has attracted much attention in the context of neurological diseases.However,none of the studies have systematically clarified this field's research hotspots and evolution rules.AIM To investigate the research hotspots,evolution patterns,and future research trends in this field in recent years.METHODS We conducted a comprehensive literature search in the Web of Science Core Collection database using the following methods:(((((TS=(NFE2 L2))OR TS=(Nfe2 L2 protein,mouse))OR TS=(NF-E2-Related Factor 2))OR TS=(NRF2))OR TS=(NFE2L2))OR TS=(Nuclear factor erythroid2-related factor 2)AND(((((((TS=(neurological diseases))OR TS=(neurological disorder))OR TS=(brain disorder))OR TS=(brain injury))OR TS=(central nervous system disease))OR TS=(CNS disease))OR TS=(central nervous system disorder))OR TS=(CNS disorder)AND Language=English from 2010 to 2022.There are just two forms of literature available:Articles and reviews.Data were processed with the software Cite-Space(version 6.1.R6).RESULTS We analyzed 1884 articles from 200 schools in 72 countriesegions.Since 2015,the number of publications in this field has increased rapidly.China has the largest number of publications,but the articles published in the United States have better centrality and H-index.Among the top ten authors with the most published papers,five of them are from China,and the author with the most published papers is Wang Handong.The institution with the most articles was Nanjing University.To their credit,three of the top 10 most cited articles were written by Chinese scholars.The keyword co-occurrence map showed that"oxidative stress","NRF2","activation","expression"and"brain"were the five most frequently used keywords.CONCLUSION Research on the role of NRF2 in neurological diseases continues unabated.Researchers in developed countries published more influential papers,while Chinese scholars provided the largest number of articles.There have been numerous studies on the mechanism of NRF2 transcription factor in neurological diseases.NRF2 is also emerging as a potentially effective target for the treatment of neurological diseases.However,despite decades of research,our knowledge of NRF2 transcription factor in nervous system diseases is still limited.Further studies are needed in the future. 展开更多
关键词 Nuclear factor erythroid 2-related factor 2 Nervous system diseases Brain Expression Activation Ferroptosis
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Role of NRF2 in regulating oxidative stress and alleviating mitochondrial and endoplasmic reticulum structural damage in heatstroke-induced brain injury 认领 引用
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作者 Bingling Yin Haiyang Guo +8 位作者 Yu Shao Chongxiao Xu Yueli Zhao Ting Chen Xuan He Shan Sun Caoyuan Wu Guodong Lin Zhiguo Pan 《World Journal of Emergency Medicine》 SCIE CAS CSCD 2026年第2期113-125,共13页
BACKGROUND:The central nervous system is a critical target of severe heatstroke,with oxidative stress and multi-organelle damage being the key pathogenic mechanisms.However,research on endogenous antioxidant defense r... BACKGROUND:The central nervous system is a critical target of severe heatstroke,with oxidative stress and multi-organelle damage being the key pathogenic mechanisms.However,research on endogenous antioxidant defense remains limited.In this study,we aimed to characterize neuronal oxidative damage as a key heatstroke pathological mechanism and assess the neuroprotective effects of nuclear factor E2-related factor 2(NRF2).METHODS:After developing in vivo and in vitro heatstroke models,we employed histological staining,cell viability and apoptosis assays,oxidative stress indicators determination,organelle ultrastructural observation,and molecular expression analysis to investigate the mechanisms of brain injury and changes in the NRF2 pathway following heatstroke.We pretreated mice and SH-SY5Y cells with tert-butylhydroquinone(TBHQ) to activate NRF2 expression.Furthermore,we utilized NRF2 knockout(KO) mice and NRF2 siRNA transfection to suppress NRF2 expression,thereby examining the effects of NRF2 both in vivo and in vitro.RESULTS:We found that heatstroke induced neuronal damage,elevated oxidative stress levels,and caused structural damage to both the mitochondria and the endoplasmic reticulum(ER).Notably,NRF2 activation was insufficient post-heatstroke.Pretreatment with TBHQ effectively activated the NRF2 signaling pathway and mitigated the resulting damage.In contrast,these injuries were exacerbated in NRF2 KO mice and SH-SY5Y cells transfected with NRF2 siRNA.CONCLUSION:This preliminary research shows that the NRF2 antioxidant signaling pathway exerts a protective effect against oxidative stress,mitigating both mitochondrial and ER structural damage in neuronal cells during heatstroke.Therefore,targeting the NRF2 pathway is a promising therapeutic strategy for heatstroke-induced neuronal injury. 展开更多
关键词 Heatstroke Endoplasmic reticulum Reactive oxygen species Antioxidants Mitochondria Nuclear factor E2-related factor 2
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