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The ameliorative effects of ginger against heat-induced oxidative stress and mitochondrial dysfunction in Caenorhabditis elegans 认领 引用 被引量：1
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作者 Tingting Xu Mingfang Tao +6 位作者 Rong Li Shuxin Tang Yuting Huang Ting Wu Senem Kamiloglu Siyi Pan Xiaoyun Xu 《Food Science and Human Wellness》 SCIE CAS CSCD 2026年第4期1823-1838,共16页
Ginger,rich in gingerols and shogaols,exhibits multiple biological properties.However,the mechanisms underlying its thermotolerance remain unclear.The study employed network pharmacology and experimental validation in... Ginger,rich in gingerols and shogaols,exhibits multiple biological properties.However,the mechanisms underlying its thermotolerance remain unclear.The study employed network pharmacology and experimental validation in Caenorhabditis elegans to investigate how gingerol-related compounds within ginger extract(GE)mitigated damage caused by heat stress(HS).A total of 18 types of gingerol analogues were identified in GE,among which 6-,8-,and 10-gingerol,as well as 6-,8-,and 10-shogaol were quantified.Collectively,these 6 compounds accounted for 54.4%of the total composition.Supplementation with 15μg/m L GE significantly extended heatstress lifespan by 20.30%,while the combination of the 6 major gingerols and shogaols at the same concentration prolonged lifespan by 18.93%.Additionally,pretreatment with GE and the combination alleviated HS-induced oxidative damage by eliminating reactive oxygen species(ROS)and upregulating antioxidant enzymes.Network pharmacology analysis suggested that the MAPK pathway may play a crucial role in thermotolerance.Experimental findings confirmed that ginger attenuated oxidative damage through the activation of SKN-1/Nrf2 and DAF-16/FOXO via the MAPK pathway.Moreover,GE stabilized mitochondrial membrane potential and restored ATP levels,thus preserving mitochondrial function during heat exposure.Further investigations using molecular docking and molecular dynamics simulations revealed that shogaols,with more stable binding affinities for Keap1 protein,exhibited more potent effects than gingerols in prolonging lifespan and reducing ROS levels under HS conditions.In short,gingerol analogues from ginger conferred thermal resistance to nematodes by mitigating oxidative damage and mitochondrial dysfunction. 展开更多
关键词 Ginger Gingerols Shogaols Thermal tolerance Oxidative stress Mitochondrial dysfunction
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Resistance exercise alleviates skeletal muscle atrophy through reduction of oxidative stress via Sestrin1 in C57BL/6J mice 认领 引用 被引量：1
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作者 Xuege Yang Jinglin Peng +3 位作者 Yating Huang Sujuan Liu Yanmei Niu Li Fu 《Sports Medicine and Health Science》 CAS CSCD 2026年第1期50-60,共11页
Resistance exercise has been confirmed to be important for maintaining muscle mass and function.However,despite considerable experimental studies,the underlying mechanisms still requires further investigation to be el... Resistance exercise has been confirmed to be important for maintaining muscle mass and function.However,despite considerable experimental studies,the underlying mechanisms still requires further investigation to be elucidated.Sestrin1 is a stress-inducible protein strongly associated with the occurrence and development of skeletal muscle dysfunction.Besides,oxidative stress is believed to be a major pathogenic mechanism in the development of skeletal muscle atrophy,whereas regular exercise training induces the endogenous antioxidative system and protects the body against adverse effects of oxidative stress.Nevertheless,whether Sestrin1 is involved in the amelioration of resistance exercise on muscle atrophy and the role of its antioxidant function in this process remains unknown.Here we show that six-week resistance exercise training significantly improved muscle function,muscle mass,and oxidative damage and maintained the level of Sestrin1 in dexamethasone-treated C57BL/6J mice.Mechanistically,Sestrin1 overexpression rescued protein degradation and oxidative stress in atrophied myotubes.Furthermore,an emerging regulator of cellular defense against toxic and oxidative insults,nuclear factor erythroid2–related factor 2(Nrf2)controls the basal and induced expression of an array of antioxidant response element–dependent genes to regulate the pathophysiological outcomes of oxidant exposure.In this study,we found that Nrf2 is a target of Sestrin1,and Nrf2 nuclear translocation is facilitated by Sestrin1.ML385(an Nrf2 inhibitor)treatment mitigated the regulatory effects of overexpression-Sestrin1.Therefore,Sestrin1 was involved in the process of resistance exercise against skeletal muscle atrophy,which may be closely related to its antioxidant capacity,revealing a potential therapeutic strategy for reducing the loss of skeletal muscle. 展开更多
关键词 Resistance exercise Muscle atrophy Sestrin1 Oxidative stress Nrf2
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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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Systematic review of mitochondrial dysfunction and oxidative stress in aging:A focus on neuromuscular junctions 认领 引用
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作者 Senlin Chai Ning Zhang +8 位作者 Can Cui Zhengyuan Bao Qianjin Wang Wujian Lin Ronald Man Yeung Wong Sheung Wai Law Rebecca Schönmehl Christoph Brochhausen Wing Hoi Cheung 《Neural Regeneration Research》 SCIE CAS CSCD 2026年第5期1947-1960,共14页
Mitochondrial dysfunction and oxidative stress are widely regarded as primary drivers of aging and are associated with several neurodegenerative diseases.The degeneration of motor neurons during aging is a critical pa... Mitochondrial dysfunction and oxidative stress are widely regarded as primary drivers of aging and are associated with several neurodegenerative diseases.The degeneration of motor neurons during aging is a critical pathological factor contributing to the progression of sarcopenia.However,the morphological and functional changes in mitochondria and their interplay in the degeneration of the neuromuscular junction during aging remain poorly understood.A defined systematic search of the Pub Med,Web of Science and Embase databases(last accessed on October 30,2024)was conducted with search terms including'mitochondria','aging'and'NMJ'.Clinical and preclinical studies of mitochondrial dysfunction and neuromuscular junction degeneration during aging.Twentyseven studies were included in this systematic review.This systematic review provides a summary of morphological,functional and biological changes in neuromuscular junction,mitochondrial morphology,biosynthesis,respiratory chain function,and mitophagy during aging.We focus on the interactions and mechanisms underlying the relationship between mitochondria and neuromuscular junctions during aging.Aging is characterized by significant reductions in mitochondrial fusion/fission cycles,biosynthesis,and mitochondrial quality control,which may lead to neuromuscular junction dysfunction,denervation and poor physical performance.Motor nerve terminals that exhibit redox sensitivity are among the first to exhibit abnormalities,ultimately leading to an early decline in muscle strength through impaired neuromuscular junction transmission function.Parg coactivator 1 alpha is a crucial molecule that regulates mitochondrial biogenesis and modulates various pathways,including the mitochondrial respiratory chain,energy deficiency,oxidative stress,and inflammation.Mitochondrial dysfunction is correlated with neuromuscular junction denervation and acetylcholine receptor fragmentation,resulting in muscle atrophy and a decrease in strength during aging.Physical therapy,pharmacotherapy,and gene therapy can alleviate the structural degeneration and functional deterioration of neuromuscular junction by restoring mitochondrial function.Therefore,mitochondria are considered potential targets for preserving neuromuscular junction morphology and function during aging to treat sarcopenia. 展开更多
关键词 aging mitochondrial dysfunction neuromuscular junction oxidative stress sarcopenia systematic review
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Evaluating quinoline's genotoxic potential:A study on hepatocyte oxidative damage and DNA stability 认领 引用
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作者 Shuqi Guo Yuze Li +5 位作者 Guidong Gao Yanmei Lei Xiangxiang Li Wansong Zong Shaoyang Hu Rutao Liu 《Journal of Environmental Sciences》 SCIE EI CAS CSCD 2026年第8期539-547,共9页
Quinoline is a heterocyclic aromatic compound with ecotoxicity,but the evidence of its toxic effects is insufficient.Through acute exposure of primary hepatocytes,combined with in vitro cytotoxicity and molecular dock... Quinoline is a heterocyclic aromatic compound with ecotoxicity,but the evidence of its toxic effects is insufficient.Through acute exposure of primary hepatocytes,combined with in vitro cytotoxicity and molecular docking simulation,the dual pathway mechanism induced by quinoline:Reactive oxygen species(ROS)-mediated oxidative damage and interaction with DNA was studied.Quinoline exposure led to excessive production of ROS in liver cells,resulting in lipid peroxidation and depletion of antioxidant defenses.Mitochondrial dysfunction intensified the production of ROS,formed a loop of self-amplification,and suppressed the repair ability of DNA.Spectroscopic analysis and molecular docking confirmed that quinoline may stabilize the embedding and binding of quinoline through π-H,H-receptor and hydrophobic force,and enhance the genotoxicity potential.The direct interaction between quinoline and DNA induced oxidative DNA damage and chain breakage,which was verified by ultraviolet spectrum decoloration,fluorescence enhancement and circular dichroism signal change.The above results confirmed that the stability of hepatocyte genome was destroyed,which provided a basis for toxicity evaluation and risk assessment of quinoline analogues. 展开更多
关键词 Quinoline Primary hepatocytes DNA damage Oxidative stress Molecular docking
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Male testosterone synthesis disorders:oxidative stress pathways,regulatory mechanisms,potential of antioxidant therapy,and botanical medicine prospects 认领 引用
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作者 Hui Wu Min-Tao Jian +5 位作者 Gang Ning Bo-Nan Li A-Jian Peng Hao-Yu Wang Xue Tang Xing Zhou 《Asian Journal of Andrology》 SCIE CAS CSCD 2026年第4期369-381,共13页
Testosterone,one of the most important hormones in men,regulates many physiological and pathological processes.Testosterone biosynthesis mainly occurs in Leydig cells.Oxidative stress(OS)is also commonly observed in L... Testosterone,one of the most important hormones in men,regulates many physiological and pathological processes.Testosterone biosynthesis mainly occurs in Leydig cells.Oxidative stress(OS)is also commonly observed in Leydig cells and is an important factor,leading to decreased testosterone concentrations.This review evaluates male testosterone synthesis disorders from the perspective of OS.OS impairs testosterone synthesis through multiple mechanisms,including modulating the function of the hypothalamic–pituitary–gonadal axis,reducing testicular steroid synthase activity,damaging the mitochondrial function of Leydig cells,inducing endoplasmic reticulum stress,and inhibiting Leydig cell development.A coordinated regulatory network comprising nuclear factor erythroid-2-related factor 2(Nrf2),sirtuin 1(SIRT1),peroxisome proliferator-activated receptor gamma coactivator 1-alpha(PGC-1α),and the glutathione pathway,plays an integral role in modulating testosterone biosynthesis.We summarize the therapeutic potential of antioxidants,especially botanical medicines,in mitigating Leydig cell oxidative injury and restoring testosterone biosynthesis,highlighting their promise as a novel treatment approach.Finally,the therapeutic potential of antioxidants in male disorders of testosterone synthesis,including late-onset hypogonadism,male infertility,and erectile dysfunction,is systematically reviewed and critically analyzed.This review provides a deeper understanding of the mechanisms underpinning testosterone synthesis disorders and may facilitate the development of new clinical treatments. 展开更多
关键词 antioxidant botanical medicine Leydig cells male disease oxidative stress testosterone synthesis
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Polystyrene microplastics impaired decidualization in mice via oxidative stress and inflammation and disrupted the reproductive function of their female offspring 认领 引用
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作者 Weike Li Boyin Tan +12 位作者 Jun Xiong Jiani Diao Jing Wang Jing Long Zhenyin Chen Yuguang He Xuemei Chen Fei Han Fangfang Li Junlin He Yingxiong Wang Yan Su Rufei Gao 《Journal of Environmental Sciences》 SCIE EI CAS CSCD 2026年第4期51-63,共13页
The extensive utilization of plastics has heightened concerns regarding microplastics exposure.However,the effects of polystyrene microplastics(PS-MPs)on early pregnancy remain inadequately investigated.This study aim... The extensive utilization of plastics has heightened concerns regarding microplastics exposure.However,the effects of polystyrene microplastics(PS-MPs)on early pregnancy remain inadequately investigated.This study aimed to examine the impact of PS-MPs on decidualization and embryo implantation in female mice,as well as the reproductive function of their offspring following maternal exposure to PS-MPs.We investigated the harmful effects of different PS-MPs sizes on mouse endometrial stromal cells(mESCs)during in vitro decidualization.Pregnant mice were orally given various concentrations of PS-MPs to examine their impact on decidualization.We evaluated oxidative stress and inflammation markers to understand their roles in abnormal decidualization.Additionally,we assessed potential reproductive health impacts on female offspring.Our findings indicated that 5μm PS-MPs effectively penetrated mESCs and significantly disrupted decidualization compared to smaller or larger particles.Pregnant mice that were exposed to 5μm PS-MPs at a dose of 1000 mg/(kg・day)exhibited substantial reductions in the decidual area and downregulation of decidualization markers such as BMP2.Inflammatory cytokines increased significantly in mESCs following 5μm PS-MPs exposure,and the elevated malondialdehyde levels in uterine tissue were mitigated by antioxidant treatment.Moreover,offspring exhibited decreased uterine wet weight,uterine organ coefficients,decidual areas,and expression of BMP2 due to maternal exposure to PS-MPs.These results highlighted the detrimental effects of PS-MPs on maternal decidualization and embryo implantation,suggesting a link to oxidative stress and inflammation,and maternal exposure to PS-MPs during pregnancy impaired reproductive function in offspring females. 展开更多
关键词 Polystyrene microplastics Decidualization Endometrial stromal cell Oxidative stress Inflammation Offspring
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Oxidative stress constrains avian mate choice:Experimental evidence for song-and testosterone-mediated pathways in Zebra Finches(Taeniopygia castanotis) 认领 引用
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作者 Juan Wang Ning Ding +3 位作者 Yingying Liu Fangbing Liu Qingying Guo Dongmei Wan 《Avian Research》 SCIE CAS CSCD 2026年第3期795-805,共11页
Oxidative stress is proposed as a key physiological mediator of reproduction,yet the specific pathways through which it influences avian mate choice remain poorly understood.Here,we experimentally manipulated oxidativ... Oxidative stress is proposed as a key physiological mediator of reproduction,yet the specific pathways through which it influences avian mate choice remain poorly understood.Here,we experimentally manipulated oxidative stress levels in male Zebra Finches(Taeniopygia castanotis)through BSO-induced glutathione depletion(high oxidative stress)or dietary supplementation with CoQ10(low oxidative stress).Female mate preference was then assessed in a three-choice arena,and male phenotypes—including coloration(cheek,chest,beak,flank),song characteristics(syllable duration,frequency parameters),body condition,circulating testosterone and gonadotropin-releasing hormone levels—were systematically quantified.Results showed that oxidative stress significantly reduced male attractiveness,as females spent less time with BSO-treated males(P<0.001)and exhibited a stronger preference for CoQ10-supplemented ones(P=0.01).These effects were not attributable to coloration or body conditions:although multiple coloration parameters(cheek brightness,chest brightness,beak chroma,cheek hue)were altered(all P<0.05)and body condition(BSO:0.31±0.17,Control:-0.21±0.18,P<0.05)were improved,these changes did not directly mediate mating decisions.Piecewise structural equation modeling revealed two primary indirect pathways:a song-mediated pathway,in which oxidative stress impaired song structure(t=-2.685,P=0.009),thereby reducing attractiveness;and a testosterone-mediated pathway,in which stress induced testicular damage and lowered testosterone levels(t=-2.311,P=0.024),further diminishing male appeal.This multifaceted assault,from internal physiological state to external secondary sexual traits,collectively diminishes overall male attractiveness.Our study provides a comprehensive mechanistic account of how oxidative stress acts as a potent physiological constraint on sexual selection,advancing insight into the physiological constraints affecting sexual selection. 展开更多
关键词 Mate choice Oxidative stress Plumage color Song characteristics Testosterone levels
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Integrating bulk and single-cell transcriptome profiling to uncover diagnostic biomarkers and regulatory mechanisms of oxidative stress in spinal cord injury 认领 引用
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作者 Jianfeng Li Kuileung Tong +9 位作者 Jiaxiang Zhou Shiming Li Zhongyuan He Fuan Wang Hongkun Chen Haizhen Li Gang Cheng Junhong Li Zhiyu Zhou Manman Gao 《Neural Regeneration Research》 SCIE CAS CSCD 2026年第6期2643-2657,共15页
Oxidative stress significantly contributes to secondary damage after spinal cord injury.Despite its importance,research on oxidative stress in spinal cord injury remains limited.Investigating the expression and regula... Oxidative stress significantly contributes to secondary damage after spinal cord injury.Despite its importance,research on oxidative stress in spinal cord injury remains limited.Investigating the expression and regulation of oxidative stress-related genes could enhance the diagnosis and treatment of spinal cord injury.In this study,we analyzed the sequencing data of human blood samples and injured mouse spinal cord tissue that were sourced from GEO databases and identified diagnostic biomarkers associated with the severity of spinal cord injury.We also explored the expression patterns of oxidative stress-related genes,potential regulatory mechanisms,and therapeutic drugs.To validate our findings,we performed immunofluorescence and quantitative polymerase chain reaction to assess gene expression in the injured spinal cord.Our results revealed biomarkers associated with oxidative stress and immune responses across different levels of spinal cord injury in humans.We identified differentially expressed oxidative stress-related genes and key hub genes in injured mouse spinal cord tissue and revealed their temporal expression patterns at both the tissue and single-cell levels.We also clarified the signaling pathways associated with oxidative stress and identified ligand-receptor pairs among various cell types at different time points after injury.Furthermore,we discovered microRNAs,long non-coding RNAs,and transcription factors that regulate these hub genes and revealed their roles in modulating gene expression at various stages after spinal cord injury.We also identified drugs targeting these hub genes.The findings from this study not only aid in identifying diagnostic biomarkers that reflect the severity of spinal cord injury,but also provide insights into the expression dynamics of oxidative stress-related genes.In addition,the study reveals potential regulatory mechanisms and identifies potential drugs to treat patients with spinal cord injury. 展开更多
关键词 bioinformatics analysis diagnostic biomarker drug intervention expression characteristics immune change oxidative stress regulation mechanism severity of the illness spinal cord injury spinal cord repair
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Chrysin alleviates pressure overload-induced myocardial remodeling through regulating the PI3K/AKT/NRF2 pathway-mediated oxidative stress response 认领 引用
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作者 Yijia Wang Xing Feng +10 位作者 Shuhui Zhao Yuchong Fu Ao Zhang Xiaofeng Shen Bowen Yu Yihao Wang Jiahui Lin Bing Zhang Weiping Ji Lianpin Wu Xiaoling Guo 《Animal Models and Experimental Medicine》 CAS CSCD 2026年第7期1373-1394,共22页
Background:Oxidative stress plays a pivotal role in the pathogenesis of heart failure and is closely linked to myocardial remodeling,which includes myocardial hypertrophy and fibrosis.Chrysin(CHR)has multiple medicina... Background:Oxidative stress plays a pivotal role in the pathogenesis of heart failure and is closely linked to myocardial remodeling,which includes myocardial hypertrophy and fibrosis.Chrysin(CHR)has multiple medicinal effects such as antioxidant,anti-inflammatory,and anti-apoptosis.This research seeks to investigate whether CHR can protect against pressure overload-induced myocardial remodeling and to explore the underlying mechanism.Methods:Transverse aortic constriction(TAC)surgery was conducted to establish a model of cardiac hypertrophy on male C57BL/6J mice.A model of cardiomyocyte hypertrophy in H9C2 cells induced by angiotensin Ⅱ(AngⅡ)was also established.Results:The results showed that CHR significantly improved survival and cardiac function,reduced myocardial hypertrophy and fibrosis,inhibited the expression of inflammatory mediators TNF-α and IL-1β,suppressed cell apoptosis rate,downregulated the levels of Bcl-2 Associated X protein(BAX)and Cleaved-Caspase-3,and upregulated B-cell lymphoma/leukemia 2(BCL-2)expression in TAC surgical mice or AngⅡ-treated H9C2 cells.CHR could also upregulate the levels of antioxidant enzymes SOD1 and HO-1 by mediating the nuclear translocation and expression of NRF2 to counteract oxidative stress response.The further mechanism investigation utilizing bioinformatics analysis and western blot revealed that the disease of heart failure is associated with the phosphatidylinositol-3-kinase(PI3K)/serinehreonine-protein kinase B(AKT)signaling pathway.Conclusions:Collectively,our findings demonstrated that CHR might exert the improvement effects on pressure overload-induced myocardial remodeling with hypertrophy and fibrosis through regulating the PI3K/AKT/NRF2 pathway-mediated oxidative stress response to alleviate myocardial cell inflammation and apoptosis,suggesting that CHR may be a promising therapeutic agent for cardiac diseases induced by pressure overload. 展开更多
关键词 apoptosis chrysin inflammation myocardial remodeling oxidative stress
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Identification and verification of key genes related to oxidative stress in type 2 diabetes and screening of candidate drugs from Traditional Chinese Medicine 认领 引用
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作者 HU Jingnan LIAO Man +3 位作者 XI Zhongwen SONG Jing WANG Yining HE Tao 《Journal of Traditional Chinese Medicine》 SCIE CAS CSCD 2026年第2期350-359,共10页
OBJECTIVE:To identify oxidative stress(OS)-related genes involved in type 2 diabetes mellitus(T2DM)and screen potential Traditional Chinese Medicine(TCM)candidates for therapeutic use.METHODS:Gene expression data from... OBJECTIVE:To identify oxidative stress(OS)-related genes involved in type 2 diabetes mellitus(T2DM)and screen potential Traditional Chinese Medicine(TCM)candidates for therapeutic use.METHODS:Gene expression data from the GSE23343 dataset were obtained from the Gene Expression Omnibus(GEO)database.Differentially expressed genes(DEGs)between healthy and T2DM patients were identified.Weighted gene co-expression network analysis(WGCNA)was performed to select modules highly correlated with clinical traits,and core genes within these modules were identified.OS-related genes were retrieved from the Gene Cards database,and the overlapping DEGs,WGCNA genes,and OS-related genes were considered as hub genes in OS-related T2DM.These hub genes were validated in GSE15653 dataset.Potential TCMs were identified by mapping the hub genes to the Coremine Medical database.In vivo validation was performed using a T2DM rat model established by a high-fat diet and streptozotocin injection.The effects of Wedelolactone were evaluated by assessing gene expression via real-time quantitative reverse transcription PCR(q RT-PCR)and Western blot,alongside metabolic and liver function parameters,including fasting blood glucose,glycated serum protein,insulin resistance,and lipid profiles.RESULTS:A total of 394 DEGs(136 up-regulated and 258 down-regulated DEGs.)were identified in the GSE23343 cohort.WGCNA results showed that the turquoise module(cor=-0.56,P=0.02)and the brown module(cor=0.66,P=0.004)were the most correlated with T2DM.Six hub genes[interleukin 33(IL33),S100 calcium binding protein A8(S100A8),Golgi membrane protein 1(GOLM1),small nuclear ribonucleoprotein U1 subunit 70(SNRNP70),hepatocyte growth factor activator(HGFAC),and oxidative stress induced growth inhibitor 1(OSGIN1)]were identified,with IL33,S100A8,and GOLM1 being up-regulated,and SNRNP70,HGFAC,and GOLM1 being down-regulated.These genes distinguished T2DM from healthy controls with AUC values greater than 0.8.Experimental verification using a T2DM rat model confirmed the expression patterns of the hub genes.In vivo data demonstrated that Wedelolactone significantly reduced oxidative stress,inflammation hepatic lipid accumulation,and improved metabolic parameters such as fasting blood glucose,glycated serum protein,and insulin resistance.CONCLUSION:These findings highlight the critical roles of IL33,S100A8,GOLM1,SNRNP70,HGFAC,and OSGIN1 as biomarkers in OS-related T2DM and suggest that Wedelolactone may be a promising TCM-based therapeutic candidate for T2DM. 展开更多
关键词 diabetes mellitus,type 2 oxidative stress gene expression profiling computational biology medicine,Chinese traditional Wedelolactone
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Oxidative cracking performance of low maturity shales at different O2 concentrations 认领 引用
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作者 Tao Wan Xiao Zhang +1 位作者 Ji-Xiang He Yan Dong 《Petroleum Science》 SCIE EI CAS CSCD 2026年第5期2833-2845,共13页
Conventional in-situ conversion technologies including electrical heating or injection of hot fluid face development challenges.Low heat transfer efficiency and limited pore expansion restrict its wide applications.Ma... Conventional in-situ conversion technologies including electrical heating or injection of hot fluid face development challenges.Low heat transfer efficiency and limited pore expansion restrict its wide applications.Maintaining uniform heatpropagation in heterogeneous shaleformations remains problematic.This study investigates the cracking behavior of low-maturity organic-rich shales under inert(N2)and oxidative(air)atmospheres,aiming to evaluate the effects of oxygen participation on reaction kinetics,pore structure evolution,and oilyield efficiency.Usingintegrated characterization techniques—including thermogravimetry(TG/DSC),X-ray diffraction(XRD),nitrogen adsorptiondesorption,nuclear magnetic resonance(NMR),and scanning electron microscopy(SEM)—the authors demonstratethat oxidative pyrolysis significantly alters shale transformation pathways.Key findings reveal that oxygenshifts kerogen cracking to lower temperatures and enhances pore development through oxidative consumption of residual carbon,which promotes micropore expansion and connectivity,ultimately increasing total porosity by 18.9%at 600°C.Oil yield experimentsshow peak production at 450°C in air,attributed to accelerated organic matter conversion,while higher temperatures(>500°C)trigger secondary cracking that reduces yields.These results highlight the potential of controlled oxidative pyrolysis for improving in-situ shale oil recovery efficiency while minimizing energy consumption. 展开更多
关键词 Low maturity shale oil Oxidative cracking Mechanical behavior Oil yield
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Transcriptome reveals probiotics mitigating MCLR-induced reproductive toxicity in male zebrafish:Regulation of reproductive endocrine,oxidative stress,and inflammatory response 认领 引用
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作者 Haoling Liu Wei Sang +8 位作者 Zixuan Liao Junli Zuo Ning Luan Xiaolin Liu Juan Chen Qing Yang Tien-Chieh Hung Qin Wu Guangyu Li 《Journal of Environmental Sciences》 SCIE EI CAS CSCD 2026年第8期411-424,共14页
Microcystin-LR(MCLR)is widely distributed in aquatic ecosystems,exhibiting strong reproductive toxicity to male fish.Several previous studies have reported probiotics could mitigate reproductive system damage caused b... Microcystin-LR(MCLR)is widely distributed in aquatic ecosystems,exhibiting strong reproductive toxicity to male fish.Several previous studies have reported probiotics could mitigate reproductive system damage caused by environmental pollutants.Whether MCLR-induced negative effects on reproduction could be mitigated by probiotics and the mechanisms involved are little studied.In this study,adult male zebrafish(Danio rerio)received MCLR exposure for 28 days,supplemented or not with the probiotic Lactobacillus rhamnosus GG(LGG).The results showed MCLR exposure impaired male zebrafish reproductive function,evidenced by reduced sperm motility and density,and testicular damage;LGG supplementation mitigated these effects.To investigate the underlying mechanisms,we performed transcriptomic analysis and evaluated the protective effects of LGG in terms of reproductive endocrinology,oxidative stress and inflammatory responses.The results indicated LGG mitigated those injury in male zebrafish by regulating sex hormone synthesis genes,the Nrf2(NF-E2-related factor2)/ARE(antioxidant response element)pathway,and the TLR4(toll-like receptor 4)/NF-κB(nuclear factor-κB)pathway,respectively.Transcriptomic analysis provides evidence that apoptotic regulation may also contribute to the mitigation of MCLR-induced reproductive toxicity.The present study validates a new approach to effectively control the MCLR-induced reproductive toxicity. 展开更多
关键词 Microcystin-LR(MCLR) Lactobacillus rhamnosus GG Reproductive toxicity Oxidative stress Inflammatory response Apoptotic
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Low-Loading Gold Nanoclusters on Zinc Oxide Enable Efficient Photocatalytic Oxidative Coupling of Methane 认领 引用
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作者 Xiaotong Zhang Tingxuan Ran +3 位作者 Jiaqi Zhao Lingsong Wang Run Shi Tierui Zhang 《Transactions of Tianjin University》 EI CAS 2026年第2期118-127,共10页
Photocatalytic oxidative coupling of methane(POCM)is a promising strategy for the production of sustainable C2+hydrocarbons;however,it typically relies on large quantities of noble metals,such as gold,to serve as a... Photocatalytic oxidative coupling of methane(POCM)is a promising strategy for the production of sustainable C2+hydrocarbons;however,it typically relies on large quantities of noble metals,such as gold,to serve as active sites for methyl coupling.In this study,we demonstrate that ZnO-supported gold nanoclusters with an average diameter of 1.1 nm provide a robust alternative to conventional gold nanoparticles,enabling efficient POCM even at ultralow gold loadings of 0.1 wt%.The optimized photocatalyst affords a C2–C4 hydrocarbon production rate of 3.89 mmol/(g h)with 94.8%selectivity under 365 nm irradiation in a batch reactor.Results reveal that the abundant interfaces between highly dispersed gold nanoclusters and ZnO substrates facilitate charge carrier separation and promote a light-induced Mars–van Krevelen reaction pathway.Methyl adsorption causes gold nanoclusters to exhibit a more intense d-σhybridization state compared to gold nanoparticles,enhancing electron transfer interactions and substantially reducing the transition-state energy barrier for methyl coupling. 展开更多
关键词 Photocatalysis Oxidative coupling of methane Nanoclusters Zinc oxide Natural gas
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Exendin-4 Inhibits High Glucose-induced Oxidative Stress in Pancreaticβ-Cell by Regulating Grx/GSH System Related Antioxidant Activity 认领 引用
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作者 XU Jing LIU Sen-Yang +5 位作者 WANG Xu-Feng SUI Hui-Xin ZHANG Chun-Jing SUN Zhao-Jie CHENG Hao QI Xiao-Dan 《中国生物化学与分子生物学报》 CAS CSCD 北大核心 2026年第4期688-696,共9页
Exendin-4(Exe),a glucagon-like peptide-1(GLP-1)receptor agonist,has a protective effect on pancreaticβcells;however,its underlying mechanism is not well understood.In this study,Exendin-4 exhibited a higher antioxida... Exendin-4(Exe),a glucagon-like peptide-1(GLP-1)receptor agonist,has a protective effect on pancreaticβcells;however,its underlying mechanism is not well understood.In this study,Exendin-4 exhibited a higher antioxidant ability and protected MIN6 cells from high glucose-induced oxidative damage by reducing reactive oxygen species(ROS)production(P<0.01),and maintaining mitochondrial function in pancreaticβcells.The beneficial effects of Exendin-4 included increased cell viability(P<0.05)and insulin secretion(P<0.05),as well as improved mitochondrial membrane potential(MMP)(P<0.01)and ATP levels(P<0.05).Additionally,Exendin-4 inhibited lactate dehydrogenase(LDH)activity(P<0.001)and reduced intracellular malondialdehyde(MDA)levels(P<0.01),and boosted the activities of antioxidant enzymes such as superoxide dismutase(SOD)(P<0.01)and catalase(CAT)(P<0.01).Glutaredoxins(Grxs)were identified as glutathione(GSH)-dependent oxidoreductases,and the Grx/GSH system is commonly referred to as the cellular antioxidant system acting in the defense of pancreaticβcells against oxidative stress and the mitochondrial damage.Our findings revealed that Exendin-4 significantly enhanced the protein expression levels of glutaredoxin 1(Grx1),glutaredoxin 2(Grx2)and glutathione reductase(GR)(P<0.05),and improved the GSH/GSSG ratio(P<0.01)and NADPH/NADP+ratio(P<0.05).These results indicate that Exendin-4 improved the function of pancreatic cells under high glucose condition.The underlying mechanism involves increasing the expression levels of key proteins in the glutaredoxin system and inhibiting the dysfunction of the Grx/GSH system,thereby reducing mitochondrial oxidative damage and functional disorders. 展开更多
关键词 exendin-4(Exe) pancreaticβ-cell high glucose(HG) oxidative stress(OS) glutaredoxins(Grxs)
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Cold-Induced Accumulation of Low-Molecular-Weight Dehydrins in Etiolated Wheat Seedlings:Relationship with Oxidative Stress Protection and Frost Tolerance 认领 引用
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作者 Tetiana O.Yastreb Pavel Vítámvás +3 位作者 Ilja T.Prášil Zdeněk Cit Ivan V.Shakhov Yuriy E.Kolupaev 《Phyton-International Journal of Experimental Botany》 SCIE 2026年第3期270-284,共15页
Low temperature is a major abiotic stress factor inducing the accumulation of dehydrins in plants.Dehydrins are hydrophilic,heat-stable proteins implicated in plant stress responses;however,their synthesis under cold ... Low temperature is a major abiotic stress factor inducing the accumulation of dehydrins in plants.Dehydrins are hydrophilic,heat-stable proteins implicated in plant stress responses;however,their synthesis under cold conditions during the early stages of wheat development has not been sufficiently studied.This study investigated the relationship between cold-induced dehydrin accumulation in etiolated seedlings and frost tolerance in wheat cultivars differing in their level of frost tolerance.Three-day-old seedlings of high frost-tolerant(high-FT)cultivars(Antonivka,Doskonala,and Nordika)and low frost-tolerant(low-FT)cultivars(Tobak,Tonnage,and Altigo)of Triticum aestivum L.were hardened at+3℃ for six days.Dehydrin accumulation was analyzed by electrophoretic separation,while frost tolerance was assessed based on seedling survival following freezing at−4,−9,and−12℃.Cold-induced oxidative damage was evaluated by determining malondialdehyde(MDA)content in seedling shoots after freezing at−4℃.In control seedlings,dehydrins were barely detectable in all cultivars.Cold hardening at+3℃ induced pronounced accumulation of dehydrins with molecular masses of approximately 46,49.6,and 68 kDa in both high-FT and low-FT cultivars.In contrast,low-molecular-weight dehydrins(14–16 kDa)were detected predominantly in high-FT cultivars.Seedling survival after freezing at−12℃ showed a strong positive correlation with total dehydrin content(r=0.82).Even stronger correlations were observed between the content of low-molecular-weight dehydrins(14–16 kDa)and seedling survival after freezing at−9 and−12℃(r=0.84 and 0.94,respectively).An inverse correlation was found between 14–16 kDa dehydrin content and MDA accumulation following freezing at−4℃(r=−0.87).These results indicate that low-molecular-weight dehydrins play an important role in protecting etiolated wheat seedlings from cold-induced oxidative stress and may serve as reliable biochemical markers of frost tolerance. 展开更多
关键词 Cold stress dehydrins frost tolerance oxidative stress Triticum aestivum L. wheat seedlings
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2-Amino-3-methylimidazo[4,5-f]quinoline induces oxidative stress-mediated DNA damage and apoptosis in multi-organ of zebrafish 认领 引用
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作者 Dan Li Weiye Liu +5 位作者 Yu Jiang Xiang Gao Yingshuang Lu Yan Zhang Huan Lv Shuo Wang 《Food Science and Human Wellness》 SCIE CAS CSCD 2026年第5期2168-2183,共16页
2-Amino-3-methylimidazo[4,5-f]quinoline(IQ)is one of mutagenic/carcinogenic heterocyclic amines(HCAs)found mainly in well-cooked meats.As a common HCAs,IQ can pose a health risk to animals as well as humans.However,to... 2-Amino-3-methylimidazo[4,5-f]quinoline(IQ)is one of mutagenic/carcinogenic heterocyclic amines(HCAs)found mainly in well-cooked meats.As a common HCAs,IQ can pose a health risk to animals as well as humans.However,to date,few studies have explored IQ's toxic effects on systemic health,and its relevant mechanism of toxicity has not been elucidated.In this study,we for the first time determined IQ accumulation and investigated the tissue damage of developing zebrafish.Zebrafish at one-month post-fertilization were exposed to IQ(80 ng/mL)for 35 days.Ultra performance liquid chromatography-tandem mass spectrometry(UPLC-MS/MS)analysis showed that IQ accumulated in multi-organ of zebrafish such as eye,spleen,gonad(ovary or testis),heart,intestine,kidney,muscle,liver,and brain.Our results showed that IQ exposure caused histopathological alterations in IQ-accumulated organs,which could compromise organ function.Exposure to IQ significantly inhibited antioxidant related indicators.Moreover,IQ exposure significantly increased mTOR gene levels.The immunohistochemical results further validated that IQ exposure tended to over activate mTOR.In addition,IQ exposure significantly reduced the expression of autophagy-related genes,and upregulated the expression of DNA damage and repair-related genes,which also detected the accumulation of fluorescence signal of DNA damage markerγ-H2AX.Furthermore,TUNEL assay showed that IQ exposure caused apoptosis.Our findings revealed that IQ could be taken up by developing zebrafish,and accumulate in multiple tissues,especially across the blood-brain barrier,accumulate in the brain,subsequently causing systemic tissue damage,urging us to pay attention to the control or intervention of IQ exposure and decreasing accumulated impairment to systemic health. 展开更多
关键词 2-Amino-3-methylimidazo[4,5-f]quinoline Danio rerio Ultra performance liquid chromatography-tandem mass spectrometry Oxidative stress DNA damage Apoptosis mTOR activation
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Attenuation of oxidative injury in retinal photoreceptor cells by Gouqizi(Lycii Fructus)and Danshen(Salviae Miltiorrhizae Radix et Rhizoma)through modulation of ANGPTL4 认领 引用
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作者 Jun Peng Junjiang Jiang +5 位作者 Junnan Zhong Siyi Zhou Tingyan Hu Xuyu Chen Qinghua Peng Yasha Zhou 《Digital Chinese Medicine》 CAS CSCD 2026年第2期290-301,共12页
Objective To investigate the protective effects of Gouqizi(Lycii Fructus,GQZ)-Danshen(Salviae Miltiorrhizae Radix et Rhizoma,DS)against hydrogen peroxide(H2O2)-induced oxidative injury in 661W retinal photorecep... Objective To investigate the protective effects of Gouqizi(Lycii Fructus,GQZ)-Danshen(Salviae Miltiorrhizae Radix et Rhizoma,DS)against hydrogen peroxide(H2O2)-induced oxidative injury in 661W retinal photoreceptor cells and to explore whether these effects involve angiopoietin-like 4(ANGPTL4).Methods Liquid chromatography-mass spectrometry(LC-MS)was used to identify the major components of GQZ-DS aqueous extract.An H2O2-induced oxidative injury model was established in 661W cells.Working concentrations of H2O2and GQZ-DS were determined using the cell counting kit-8(CCK-8)assay.Cells were subjected to GQZ-DS,ANGPTL4 knockdown,or ANGPTL4 overexpression as indicated.Flow cytometry was used to analyze cell cycle distribution,apoptotic rate,and intracellular reactive oxygen species(ROS).Colorimetric determination of malondialdehyde(MDA)content and superoxide dismutase(SOD)activity using the thiobarbituric acid(TBA)method was performed.The protein expression level of ANGPTL4 was assessed by immunofluorescence.Reverse transcription-quantitative polymerase chain reaction(RT-qPCR)was performed to quantify the mRNA level of ANGPTL4.Western blot was used to detect the protein levels of ANGPTL4 and cleaved caspase-3.Results LC-MS identified five major constituents in the GQZ-DS aqueous extract:2-O-β-Dglucopyranosyl-L-ascorbic acid,rutin,D-galactose,salvianolic acid A,and tanshinone IIA.The CCK-8 method selected 300μmol/L H2O2as the oxidative stress condition for experiments,and 0.05 and 0.1 g/mL were selected as the low and high doses of GQZ-DS,respectively,for subsequent experiments.The intervention with H2O2resulted in reduced cell viability,elevated ROS and MDA levels,decreased SOD activity,increased apoptotic rate,upregulated cleaved caspase-3 expression,and G0/G1 phase cell cycle arrest of 661W cells.Both low and high doses of GQZ-DS alleviated these alterations,with high dose exhibiting stronger protective effects(P<0.05 or P<0.01).GQZ-DS also downregulated ANGPTL4 expression at both the mRNA and protein levels.Following plasmid transfection of cells,the study further revealed that ANGPTL4 knockdown mitigated oxidative stress and apoptosis-related injury,whereas ANGPTL4 overexpression exacerbated these pathological changes.Moreover,GQZDS partially reversed the degree of cellular oxidative damage induced by ANGPTL4 overexpression. 展开更多
关键词 Gouqizi(Lycii Fructus)and Danshen (Salviae Miltiorrhizae Radix et Rhizoma) Retinal photoreceptor cells Angiopoietin-like 4 Oxidative injury Apoptosis
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Gomisin D alleviates podocyte injury in diabetic kidney disease by inhibiting oxidative stress via activation of the GSK3β(Ser9)/Nrf2/ARE signaling pathway 认领 引用
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作者 Ming Xiang Hai-Ying Chen Xiang-Dong Lin 《Asian Pacific Journal of Tropical Biomedicine》 SCIE CAS 2026年第8期342-353,I0001,I0002,共12页
Objective:To explore whether gomisin D,a lignan derived from Schisandra chinensis,protects against podocyte injury in diabetic kidney disease and to elucidate its underlying mechanisms.Methods:Network pharmacology was... Objective:To explore whether gomisin D,a lignan derived from Schisandra chinensis,protects against podocyte injury in diabetic kidney disease and to elucidate its underlying mechanisms.Methods:Network pharmacology was employed to analyze the potential interactions between gomisin D and podocyte injuryrelated targets in diabetic nephropathy.A high glucose-induced injury model of mouse podocyte MPC5 cells was established,and the effect of gomisin D on podocyte injury was subsequently evaluated by measurement of reactive oxygen species levels and biochemical markers and Western blotting.Molecular docking and further molecular biology assays were conducted to explore the interaction between gomisin D and the target protein.Results:Gomisin D inhibited high glucose-induced oxidative stress,improved cell viability,and preserved the expression of podocin and synaptopodin.Network pharmacology identified glycogen synthase kinase-3β(GSK3β)as a key target.Molecular docking predicted a potential interaction between gomisin D and GSK3β,which was further validated by drug affinity responsive target stability and cellular thermal shift assay,confirming direct binding in live cells.Mechanistically,gomisin D enhanced the phosphorylation of GSK3βat Ser9,promoted the nuclear translocation of nuclear factor erythroid 2-related factor 2(Nrf2),and upregulated levels of downstream antioxidant proteins heme oxygenase-1 and NAD(P)H quinone oxidoreductase 1.Furthermore,forced expression of the constitutively active GSK3βmutant S9A decreased GSK3β(Ser9)phosphorylation and reversed gomisin D-induced upregulation of these antioxidant markers.Conclusions:Gomisin D mitigates high glucose-induced podocyte injury in vitro by inhibiting oxidative stress via activation of the GSK3β(Ser9)/Nrf2/ARE signaling pathway. 展开更多
关键词 Gomisin D Diabetic kidney disease Podocyte injury GSK3β Nrf2/ARE pathway Oxidative stress
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Amomum villosum extract alleviates diabetic neuropathy via phosphoinositide 3-kinase/AKT-mediated antioxidative and antiapoptotic effects 认领 引用
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作者 Dong-Quan Kou Ming-Jie Liu +1 位作者 Xiao-Lan Gao Fu-Rong Guo 《World Journal of Diabetes》 SCIE 2026年第3期162-174,共13页
BACKGROUND Diabetic peripheral neuropathy(DPN)affects nearly half of patients with diabetes and is projected to increase substantially as the diabetes prevalence rises globally.Current treatments remain largely sympto... BACKGROUND Diabetic peripheral neuropathy(DPN)affects nearly half of patients with diabetes and is projected to increase substantially as the diabetes prevalence rises globally.Current treatments remain largely symptomatic with limited efficacy in halting disease progression.Amomum villosum Lour.(AVL),a traditional Chinese medicinal herb with anti-inflammatory and antioxidant properties,represents a potential new therapeutic candidate for DPN management.AIM To explore the therapeutic effects of the aqueous extract of AVL on DPN in rats and its underlying molecular mechanisms.METHODS A type 1 diabetic rat model was induced by streptozotocin.Pain thresholds were assessed using paw withdrawal threshold and paw withdrawal latency.Primary dorsal root ganglion(DRG)neurons were extracted and cultured to detect indicators related to oxidative stress,inflammatory response,and apoptosis.The therapeutic effects of AVL on DPN rats were evaluated using Western blotting,quantitative PCR,enzyme-linked immunosorbent assay,reactive oxygen species(ROS)content detection,terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling(TUNEL)assay,and flow cytometry.The molecular mechanisms of AVL in inhibiting oxidative stress and apoptosis via the phosphoinositide 3-kinase(PI3K)/AKT signaling pathway were also explored.RESULTS AVL treatment significantly counteracted the elevated blood glucose and reduced body weight in diabetic rats.The mechanical and thermal pain thresholds were significantly increased,indicating AVL's analgesic effects.In the diabetes mellitus(DM)+AVL group,the expression of inflammatory cytokines[tumor necrosis factor alpha,interleukin 6(IL-6),IL-1β]and malondialdehyde content in DRG tissue were lower than those in the DM+vehicle group.However,compared with the DM+vehicle group,the glutathione level was increased in the DM+AVL group.Consistently,immunofluorescence showed that the fluorescence intensity representing ROS in primary DRG neurons was also significantly reduced compared with the DM+vehicle group.In addition,flow cytometry and TUNEL assays revealed that AVL treatment markedly decreased the apoptosis rate of DRG neurons,as evidenced by downregulated caspase-3 and B-cell lymphoma 2(Bcl-2)-associated X protein expression and upregulated Bcl-2 expression,indicating that AVL also inhibits DRG neuronal apoptosis.Further mechanistic studies demonstrated that AVL treatment activated the PI3K/AKT signaling pathway in DRG neurons.However,intervention with the PI3K inhibitor LY294002 significantly reversed the therapeutic effects of AVL on DNP rats.Mechanistically,AVL activated the PI3K/AKT signaling pathway,suppressing oxidative stress and apoptosis in the DRG tissue of DNP rats.CONCLUSION AVL alleviates DNP in rats by activating the PI3K/AKT signaling pathway,inhibiting oxidative stress and apoptosis and reducing inflammatory responses.This study provides strong experimental evidence for the application of AVL in DNP treatment and offers new ideas and directions for the development of DNP treatments based on natural medicines. 展开更多
关键词 Amomum villosum Lour. Diabetic peripheral neuropathy phosphoinositide 3-kinase/AKT Oxidative stress Apoptosis
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