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强化hemE和hemQ表达对枯草芽孢杆菌合成血红素的影响 认领 引用
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作者 杨绍梅 周长旭 +5 位作者 王鹏 张同 来凤堂 李树标 薄文文 马钦元 《食品与发酵工业》 EI CAS CSCD 北大核心 2026年第12期35-42,共8页
枯草芽孢杆菌(Bacillus subtilis)作为公认安全(Generally Recognized as Safe,GRAS)菌株,是生产食品级血红素的理想底盘,但其粪卟啉依赖性(coproporphyrin-dependent,CPD)合成途径中关键酶的调控机制尚不明确。为解析并突破该途径的限... 枯草芽孢杆菌(Bacillus subtilis)作为公认安全(Generally Recognized as Safe,GRAS)菌株,是生产食品级血红素的理想底盘,但其粪卟啉依赖性(coproporphyrin-dependent,CPD)合成途径中关键酶的调控机制尚不明确。为解析并突破该途径的限速步骤,该研究系统评价了强化尿卟啉原脱羧酶(UroD,hemE编码)和粪血红素脱羧酶(ChdC,hemQ编码)的表达对血红素合成的影响。采用无标记基因修饰技术,将强组成型启动子驱动的hemE和hemQ基因分别或组合整合到B.subtilis BSH11基因组的中性位点ydaP和yvkC,构建基因过表达菌株,并通过摇瓶发酵和实时荧光定量PCR分析其血红素产量和基因转录水平。结果表明,单独强化hemE表达效果最为显著,其转录水平最高提升303倍,发酵48 h后胞外血红素产量达到(23.90±1.49)mg/L,较对照菌株提高826%;单独强化hemQ表达对产量无明显促进作用;而两基因共表达时,胞外血红素产量较hemE单过表达菌株反而下降35%。研究证实,UroD是B.subtilis血红素CPD合成途径的关键限速步骤,而ChdC的催化能力在当前条件下并非主要限制因素。该发现为后续在B.subtilis这一安全底盘中,通过精准代谢工程策略高效合成食品级血红素提供了核心靶点和理论指导。 展开更多
关键词 血红素 枯草芽孢杆菌 代谢工程 hemE基因 基因过表达
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Comparative Study of Auricularia auricula Polysaccharide-Iron Complex,Heme Iron,and Ferrous Glycinate in Iron-Deficient Adults:A Randomized Clinical Trial 认领 引用
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作者 Nurfarih Hanna Mohd Zarif Fikri Bin Mohd +1 位作者 Muhammad Nabil Fikri Bin Mohd Nurfarazuna Binti Mohd Fadrol 《Journal of Clinical and Nursing Research》 2026年第1期261-273,共13页
Iron deficiency anemia affects approximately 1.62 billion people worldwide,yet traditional iron supplements present bioavailability limitations and gastrointestinal side effects.This randomized,double-blind clinical t... Iron deficiency anemia affects approximately 1.62 billion people worldwide,yet traditional iron supplements present bioavailability limitations and gastrointestinal side effects.This randomized,double-blind clinical trial investigated a novel Auricularia auricula polysaccharide-iron complex(AAPIC)compared with heme iron and ferrous glycinate in 180 iron-deficient adults receiving 30 mg elemental iron daily for 12 weeks.AAPIC achieved comparable hemoglobin improvements(from 98.3±8.7 to 126.5±9.2 g/L)to heme iron(from 97.8±9.1 to 128.3±8.6 g/L)and was significantly superior to ferrous glycinate(from 98.6±8.9 to 119.7±10.3 g/L;p<0.001).Iron absorption efficiency showed AAPIC at 23.7±4.2%,heme iron at 25.1±3.8%,and ferrous glycinate at 18.4±5.1%.Toxicological assessments revealed no hepatotoxicity,nephrotoxicity,or mutagenicity.Gastrointestinal adverse events occurred in 8.3%of AAPIC recipients versus 15.0%with ferrous glycinate and 10.0%with heme iron.The polysaccharide component facilitates iron transport through enhanced intestinal uptake mechanisms.AAPIC represents a promising,well-tolerated alternative with clinical efficacy comparable to established iron formulations. 展开更多
关键词 Auricularia auricula polysaccharide Iron complex Heme iron Ferrous glycinate Bioavailability Iron deficiency anemia Clinical trial Toxicology
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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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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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Adipose-derived mesenchymal stromal cell secretome protects against kidney injury through induction of heme oxygenase 1 upregulation in vitro 认领 引用
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作者 Hanan Jafar Nidaa A Ababneh +5 位作者 Dana Alhattab Renata M Alatoom Suzan Zalloum Bareqa Salah Hussein Alhawari Abdalla Awidi 《World Journal of Nephrology》 2025年第3期159-170,共12页
BACKGROUND Acute kidney injury is characterized by a sudden decline in renal function,often due to ischemia or nephrotoxins,leading to increased oxidative stress and inflam-mation.AIM To investigate the protective eff... BACKGROUND Acute kidney injury is characterized by a sudden decline in renal function,often due to ischemia or nephrotoxins,leading to increased oxidative stress and inflam-mation.AIM To investigate the protective effects of adipose-derived mesenchymal stromal cell(ADMSC)secretome on renal tubular epithelial cells(NRK-52E)as an in vitro model of oxidative stress-associated kidney injury.METHODS ADMSCs were isolated from human adipose tissue and characterized for mesenchymal markers and differentiation potential.Conditioned media(CM)was collected after 48-hour serum-free culture and applied to serum-deprived NRK-52E cells for 48 hours.Cell viability was assessed using the MTT assay,apoptosis was assessed by Annexin V-FITC/PI staining and flow cytometry,reactive oxygen species(ROS)levels via H2DCFDA staining,and mitochondrial membrane potential by the tetramethylrhodamine ethyl ester assay.The expression of heme oxygenase-1(HO-1),nuclear factor erythroid 2-related factor 2(Nrf2),and NAD(P)H quinone dehydrogenase 1(Nqo1)genes was quantified by quantitative polymerase chain reaction.Comparative transcriptomic analysis was performed on ADMSCs and bone marrow-derived MSCs(BM-MSCs)using publicly available microarray data(GSE108511).RESULTS ADMSC secretome significantly reduced ROS production and enhanced mitochondrial membrane potential in NRK cells.Gene expression analysis revealed a significant upregulation of HO-1 mRNA levels in ADMSC-CM treated cells.However,no significant changes were observed in Nrf2 and Nqo1 mRNA levels.Transcriptome analysis of ADMSCs against BM-MSCs revealed significant differences in the expression of genes related to oxidative stress response,antioxidant activity,and mitochondrial function.CONCLUSION The results of this study suggest that the ADMSC secretome exerts multifaceted protective effects on NRK cells by reducing oxidative stress and enhancing mitochondrial function.The study demonstrates the potential beneficial applications of the ADMSC secretome in treating oxidative stress-related kidney injuries. 展开更多
关键词 Renal tubular epithelial cells Secretome Heme oxygenase 1 upregulation Oxidative stress Mesenchymal stromal cells Acute kidney injury
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优化GBM算法预测蛋白质-HEME结合残基 认领 引用
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作者 郭国栋 潘星宇 +2 位作者 白云霞 包梦雪 李彩艳 《中国科技论文在线精品论文》 2025年第2期198-200,共3页
为了提升蛋白质-HEME结合残基的预测精度,本文基于Gradient Boosting Machine(GBM)算法,重点优化了其内置参数,包括最小训练样本数(minobsinnode)、决策树深度(depth)、迭代次数(n.trees)和学习速率(shrinkage)。通过总结数据科学竞赛... 为了提升蛋白质-HEME结合残基的预测精度,本文基于Gradient Boosting Machine(GBM)算法,重点优化了其内置参数,包括最小训练样本数(minobsinnode)、决策树深度(depth)、迭代次数(n.trees)和学习速率(shrinkage)。通过总结数据科学竞赛中的经验,调整最优扰动权重和参数配置,成功避免过拟合问题,并实现了更高的预测精确度。在此基础上,改进采样方法以克服样本不平衡问题,结合五折交叉检验与独立检验对模型进行全面优化。 展开更多
关键词 生物物理学 GBM算法 Heme残基 加权采样法
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Production of biliverdin by biotransformation of exogenous heme using recombinant Pichia pastoris cells 认领 引用 被引量：1
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作者 Jianfeng Mei Yanchao Han +3 位作者 Shihang Zhuang Zhikai Yang Yu Yi Guoqing Ying 《Bioresources and Bioprocessing》 SCIE EI 2024年第1期263-272,共10页
Biliverdin,a bile pigment hydrolyzed from heme by heme oxygenase(HO),serves multiple functions in the human body,including antioxidant,anti-inflammatory,and immune response inhibitory activities.Biliverdin has great p... Biliverdin,a bile pigment hydrolyzed from heme by heme oxygenase(HO),serves multiple functions in the human body,including antioxidant,anti-inflammatory,and immune response inhibitory activities.Biliverdin has great potential as a clinical drug;however,no economic and efficient production method is available currently.Therefore,the production of biliverdin by the biotransformation of exogenous heme using recombinant HO-expressing yeast cells was studied in this research.First,the heme oxygenase-1 gene(HO1)encoding the inducible plastidic isozyme from Arabidopsis thaliana,with the plastid transport peptide sequence removed,was recombined into Pichia pasto-ris GS115 cells.This resulted in the construction of a recombinant P.pastoris GS115-HO1 strain that expressed active HO1 in the cytoplasm.After that,the concentration of the inducer methanol,the induction culture time,the pH of the medium,and the concentration of sorbitol supplied in the medium were optimized,resulting in a significant improvement in the yield of HO1.Subsequently,the whole cells of GS115-HO1 were employed as catalysts to convert heme chloride(hemin)into biliverdin.The results showed that the yield of biliverdin was 132 mg/L when hemin was added to the culture of GS115-HO1 and incubated for 4 h at 30°C.The findings of this study have laid a good foundation for future applications of this method for the economical production of biliverdin. 展开更多
关键词 Biliverdin Biotransformation Heme Heme oxygenase-1 Recombinant Pichia pastoris
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Overexpression of heme oxygenase-1 protects smooth muscle cells against oxidative injury and inhibits cell proliferation 认领 引用 被引量：16
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作者 MIN ZHANG, BAO HuI ZHANG, LI CHEN, WEI AN1 Institute of Sports Medicine, The Third Hospital, Peking University, Beijing 100083, China 2Department of Cell Biology, Capital University of Medical Sciences, Beijing 100054, China 《Cell Research》 SCIE CAS 2002年第2期123-132,共10页
To investigate whether the expression of exogenous heme oxygenase-1 (HO-1) gene within vascular smooth muscle cells (VSMC) could protect the cells from free radical attack and inhibit cell proliferation, we establishe... To investigate whether the expression of exogenous heme oxygenase-1 (HO-1) gene within vascular smooth muscle cells (VSMC) could protect the cells from free radical attack and inhibit cell proliferation, we established an in vitro transfection of human HO-1 gene into rat VSMC mediated by a retroviral vector. The results showed that the profound expression of HO-1 protein as well as HO activity was 1.8- and 2.0-fold increased respectively in the transfected cells compared to the non-transfected ones. The treatment of VSMC with different concentrations of H2O2 led to the remarkable cell damage as indicated by survival rate and LDH leakage. However, the resistance of the HO-1 transfected VSMC against H2O2 was significantly raised. This protective effect was dramatically diminished when the transfected VSMC were pretreated with ZnPP-IX, a specific inhibitor of HO, for 24 h. In addition, we found that the growth potential of the transfected cells was significantly inhibited directly by increased activity of HO-1, and this effect might be related to decreased phosphorylation of MAPK. These results suggest that the overexpression of introduced hHO-1 is potentially able to reduce the risk factors of atherosclerosis, partially due to its cellular protection against oxidative injury and to its inhibitory effect on cellular proliferation. 展开更多
关键词 Animals Blotting, Northern Blotting, Southern Blotting, Western Cell Division Cell Survival Cells, Cultured Cyclic GMP Dose-Response Relationship, Drug Flow Cytometry Free Radicals Genetic Vectors Heme Oxygenase (Decyclizing) Heme Oxygenase-1 Humans Hydrogen Peroxide MAP Kinase Signaling System Male Membrane Proteins Muscle, Smooth Myocytes, Smooth Muscle Oxidants Oxidative Stress Oxygen Phosphorylation Rats Rats, Sprague-Dawley Research Support, Non-U.S. Gov't Retroviridae Time Factors Transfection
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Heme in intestinal epithelial cell turnover, differentiation, detoxification, inflammation, carcinogenesis, absorption and motility 认领 引用 被引量：9
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作者 Phillip S Oates Adrian R West 《World Journal of Gastroenterology》 SCIE CAS 2006年第27期4281-4295,共15页
The gastrointestinal tract is lined by a simple epithelium that undergoes constant renewal involving cell division, differentiation and cell death. In addition, the epithelial lining separates the hostile processes of... The gastrointestinal tract is lined by a simple epithelium that undergoes constant renewal involving cell division, differentiation and cell death. In addition, the epithelial lining separates the hostile processes of digestion and absorption that occur in the intestinal lumen from the aseptic environment of the internal milieu by defensive mechanisms that protect the epithelium from being breached. Central to these defensive processes is the synthesis of heme and its catabolism by heme oxygenase （HO）. Dietary heme is also an important source of iron for the body which is taken up intact by the enterocyte. This review describes the recent literature on the diverse properties of heme/HO in the intestine tract. The roles of heme/HO in the regulation of the cell cycle/ apoptosis, detoxification of xenobiotics, oxidative stress, inflammation, development of colon cancer, hemeiron absorption and intestinal motility are specifically examined. 展开更多
关键词 Absorption Heme Uptake Release Heme oxygenase Oxidant Cytoprotection Inflammation Cancer Detoxification
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Heme oxygenase-1 protects donor livers from ischemia/reperfusion injury:The role of Kupffer cells 认领 引用 被引量：29
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作者 Zeng, Zhong Huang, Han-Fei +2 位作者 Chen, Ming-Qing Song, Fei Zhang, Yu-Jun 《World Journal of Gastroenterology》 SCIE CAS 2010年第10期1285-1292,共8页
AIM:To examine whether heme oxygenase (HO)-1 overexpression would exert direct or indirect effects on Kupffer cells activation, which lead to aggravation of reperfusion injury.METHODS: Donors were pretreated with coba... AIM:To examine whether heme oxygenase (HO)-1 overexpression would exert direct or indirect effects on Kupffer cells activation, which lead to aggravation of reperfusion injury.METHODS: Donors were pretreated with cobalt protoporphyrin (CoPP) or zinc protoporphyrin (ZnPP), HO-1 inducer and antagonist, respectively. Livers were stored at 4℃ for 24 h before transplantation. Kupffer cells were isolated and cultured for 6 h after liver reperfusion.RESULTS: Postoperatively, serum transaminases were significantly lower and associated with less liver injury when donors were pretreated with CoPP, as compared with the ZnPP group. Production of the cytokines tumor necrosis factor-α and interleukin-6 generated by Kupffer cells decreased in the CoPP group. The CD14 expression levels (RT-PCR/Western blots) of Kupffer cells from CoPP-pretreated liver grafts reduced.CONCLUSION: The study suggests that the potential utility of HO-1 overexpression in preventing ischemiaeperfusion injury results from inhibition of Kupffer cells activation. 展开更多
关键词 Heme oxygenase-1 Kupffer cells Ischemiaeperfusion injury Liver transplantation
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Quercetin protects against diabetic retinopathy in rats by inducing heme oxygenase-1 expression 认领 引用 被引量：39
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作者 Guang-Rui Chai Shu Liu +1 位作者 Hong-Wei Yang Xiao-Long Chen 《Neural Regeneration Research》 SCIE CAS CSCD 2021年第7期1344-1350,共7页
Quercetin is a widely-occurring flavonoid that protects against cancer, and improves memory and cardiovascular functions.However, whether quercetin exhibits therapeutic effects in diabetic retinopathy remains unclear.... Quercetin is a widely-occurring flavonoid that protects against cancer, and improves memory and cardiovascular functions.However, whether quercetin exhibits therapeutic effects in diabetic retinopathy remains unclear.In this study, we established a rat model of streptozocininduced diabetic retinopathy.Seventy-two hours later, the rats were intraperitoneally administered 150 mg/kg quercetin for 16 successive weeks.Quercetin markedly increased the thickness of the retinal cell layer, increased the number of ganglion cells, and decreased the overexpression of the pro-inflammatory factors interleukin-1β, interleukin-18, interleukin-6 and tumor necrosis factor-α in the retinal tissue as well as the overexpression of high mobility group box-1 and the overactivation of the NLRP3 inflammasome.Furthermore, quercetin inhibited the overexpression of TLR4 and NF-κBp65, reduced the expression of the pro-angiogenic vascular endothelial growth factor and soluble intercellular adhesion molecule-1, and upregulated the neurotrophins brain-derived neurotrophic factor and nerve growth factor.Intraperitoneal injection of the heme oxygenase-1 inhibitor zinc protoporphyrin blocked the protective effect of quercetin.These findings suggest that quercetin exerts therapeutic effects in diabetic retinopathy possibly by inducing heme oxygenase-1 expression.This study was approved by the Animal Ethics Committee of China Medical University, China(approval No.2016 PS229K) on April 8, 2016. 展开更多
关键词 angiogenesis diabetic retinopathy flavonoid heme oxygenase-1 inflammation neurotrophin quercetin repair
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Region-dependent effects of diabetes and insulin-replacement on neuronal nitric oxide synthase-and heme oxygenase-immunoreactive submucous neurons 认领 引用 被引量：1
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作者 Nikolett Bódi Zita Szalai +1 位作者 Lalitha Chandrakumar Mária Bagyánszki 《World Journal of Gastroenterology》 SCIE CAS 2017年第41期7359-7368,共10页
AIM To investigate the intestinal segment-specific effects of diabetes and insulin replacement on the density of different subpopulations of submucous neurons. METHODS Ten weeks after the onset of type 1 diabetes samp... AIM To investigate the intestinal segment-specific effects of diabetes and insulin replacement on the density of different subpopulations of submucous neurons. METHODS Ten weeks after the onset of type 1 diabetes samples were taken from the duodenum, ileum and colon of streptozotocin-induce diabetic, insulin-treated diabetic and sex-and age-matched control rats. Whole-mount preparations of submucous plexus were prepared from the different gut segments for quantitative fluorescent immunohistochemistry. The following double-immunostainings were performed: neuronal nitric oxide synthase(n NOS) and Hu C/D, heme oxygenase(HO) 1 and peripherin, as well as HO2 and peripherin. The density of n NOS-, HO1-and HO2-immunoreactive(IR) neurons was determined as a percentage of the total number of submucous neurons. RESULTS The total number of submucous neurons and the proportion of n NOS-, HO1-and HO2-IR subpopulations were not affected in the duodenal ganglia of control, diabetic and insulin-treated rats. While the total neuronal number did not change in either the ileum or the colon, the density of nitrergic neurons exhibited a 2-and 3-fold increase in the diabetic ileum and colon, respectively, which was further enhanced after insulin replacement. The presence of HO1-and HO2-IR submucous neurons was robust in the colon of controls(38.4%-50.8%), whereas it was significantly lower in the small intestinal segments(0.0%-4.2%, P < 0.0001). Under pathophysiological conditions the only alteration detected was an increase in the ileum and a decrease in the colon of the proportion of HO-IR neurons in insulin-treated diabetic animals. CONCLUSION Diabetes and immediate insulin replacement induce the most pronounced region-specific alterations of n NOS-, HO1-and HO2-IR submucous neuronal density in the distal parts of the gut. 展开更多
关键词 Nitrergic neurons Heme oxygenase 1 Heme oxygenase 2 Submucous neurons Gut regionspecificity Diabetes Insulin
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Heme oxygenase-1 as a therapeutic target in inflammatory disorders of the gastrointestinal tract 认领 引用 被引量：14
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作者 Vijith Vijayan Sebastian Mueller +1 位作者 Eveline Baumgart-Vogt Stephan Immenschuh 《World Journal of Gastroenterology》 SCIE CAS 2010年第25期3112-3119,共8页
Heme oxygenase (HO)-1 is the inducible isoform of the first and rate-limiting enzyme of heme degradation. HO-1 not only protects against oxidative stress and apoptosis, but has received a great deal of attention in re... Heme oxygenase (HO)-1 is the inducible isoform of the first and rate-limiting enzyme of heme degradation. HO-1 not only protects against oxidative stress and apoptosis, but has received a great deal of attention in recent years because ofits potent anti-inflammatory functions. Studies with HO-1 knockout animal models have led to major advances in the understanding of how HO-1 might regulate inflammatory immune responses, although little is known on the underlying mechanisms. Due to its beneficial effects the targeted induction of this enzyme is considered to have major therapeutic po- tential for the treatment ofinflammatory disorders. This review discusses current knowledge on the mechanisms that mediate anti-inflammatory protection by HO-1. More specifically, the article deals with the role of HO-1 in the pathophysiology of viral hepatitis, inflammatorybowel disease, and pancreatitis. The effects of specific HO-1 modulation as a potential therapeutic strategy in experimental cell culture and animal models of these gastrointestinal disorders are summarized. In conclusion, targeted regulation of HO-1 holds major promise for future clinical interventions in inflammatory diseases of the gastrointestinal tract. 展开更多
关键词 Antioxidant Heme oxygenase Hepatitis Immunity Inflammation Inflammatory bowel disease Oxidative stress Pancreatitis
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Rosmarinic acid elicits neuroprotection in ischemic stroke via Nrf2 and heme oxygenase 1 signaling 认领 引用 被引量：15
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作者 Hai-Ying Cui Xiang-Jian Zhang +4 位作者 Yi Yang Cong Zhang Chun-Hua Zhu Jiang-Yong Miao Rong Chen 《Neural Regeneration Research》 SCIE CAS CSCD 2018年第12期2119-2128,共10页
Rosmarinic acid（RA） can elicit a neuroprotective effect against ischemic stroke, but the precise molecular mechanism remains poorly understood. In this study, an experimental ischemic stroke model was established in... Rosmarinic acid（RA） can elicit a neuroprotective effect against ischemic stroke, but the precise molecular mechanism remains poorly understood. In this study, an experimental ischemic stroke model was established in CD-1 mice（Beijing Vital River Laboratory Animal Technology, Beijing, China） by occluding the right middle cerebral artery for 1 hour and allowing reperfusion for 24 hours. After intraperitoneally injecting model mice with 10, 20, or 40 mg/kg RA, functional neurological deficits were evaluated using modified Longa scores. Subsequently, cerebral infarct volume was measured using TTC staining and ischemic brain tissue was examined for cell apoptosis with TUNEL staining. Superoxide dismutase activity and malondialdehyde levels were measured by spectrophometry. Expression of heme oxygenase-1（HO-1）, nuclear factor erythroid 2-related factor 2（Nrf2）, Bcl-2, Bax, Akt, and phospho-Ser473 Akt proteins in ischemic brain tissue was detected by western blot, while mRNA levels of Nrf2, HO-1, Bcl-2, and Bax were analyzed using real time quantitative PCR. In addition, HO-1 enzyme activity was measured spectrophotometrically. RA（20 and 40 mg/kg） greatly improved neurological function, reduced infarct volume, decreased cell apoptosis, upregulated Bcl-2 protein and mRNA expression, downregulated Bax protein and mRNA expression, increased HO-1 and Nrf2 protein and mRNA expression, increased superoxide dismutase activity, and decreased malondialdehyde levels in ischemic brain tissue of model mice. However, intraperitoneal injection of a HO-1 inhibitor（10 mg/kg zinc protoporphyrin IX） reversed the neuroprotective effects of RA on HO-1 enzyme activity and Bcl-2 and Bax protein expression. The PI3 K/Akt signaling pathway inhibitor LY294002（10 mM） inhibited Akt phosphorylation, as well as Nrf2 and HO-1 expression. Our findings suggest that RA has anti-oxidative and anti-apoptotic properties that protect against ischemic stroke by a mechanism involving upregulation of Nrf2 and HO-1 expression via the PI3 K/Akt signaling pathway. 展开更多
关键词 cerebral ischemiaeperfusion rosmarinic acid cellular apoptosis oxidative injury neuroprotection Bcl-2 Bax Nrf2 heme oxygenase 1 PI3K/Akt signal pathway neural regeneration
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Hydrogen-rich water protects against inflammatory bowel disease in mice by inhibiting endoplasmic reticulum stress and promoting heme oxygenase-1 expression 认领 引用 被引量：11
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作者 Nai-Ying Shen Jian-Bin Bi +4 位作者 Jing-Yao Zhang Si-Min Zhang Jing-Xian Gu Kai Qu Chang Liu 《World Journal of Gastroenterology》 SCIE CAS 2017年第8期1375-1386,共12页
AIM To investigate the therapeutic effect of hydrogen-rich water(HRW) on inflammatory bowel disease(IBD) and to explore the potential mechanisms involved.METHODS Male mice were randomly divided into the following four... AIM To investigate the therapeutic effect of hydrogen-rich water(HRW) on inflammatory bowel disease(IBD) and to explore the potential mechanisms involved.METHODS Male mice were randomly divided into the following four groups: control group, in which the mice received equivalent volumes of normal saline(NS) intraperitoneally(ip); dextran sulfate sodium(DSS) group, in which the mice received NS ip(5 m L/kg body weight, twice per day at 8 am and 5 pm) for 7 consecutive days after IBD modeling; DSS + HRW group, in which the mice received HRW(in the same volume as the NS treatment) for 7 consecutive days after IBD modeling; and DSS + HRW + Zn PP group, in which the mice received HRW(in the same volume as the NS treatment) and ZnP P [a heme oxygenase-1(HO-1) inhibitor, 25 mg/kg] for 7 consecutive days after IBD modeling. IBD was induced by feeding DSS to the mice, and blood and colon tissues were collected on the 7th d after IBD modeling to determine clinical symptoms, colonic inflammation and the potential mechanisms involved.RESULTS The DSS + HRW group exhibited significantly attenuated weight loss and a lower extent of disease activity index compared with the DSS group on the 7th d(P < 0.05). HRW exerted protective effects against colon shortening and colonic wall thickening in contrast to the DSS group(P < 0.05). The histological study demonstrated milder inflammation in the DSS + HRW group, which was similar to normal inflammatory levels, and the macroscopic and microcosmic damage scores were lower in this group than in the DSS group(P < 0.05). The oxidative stress parameters, including MDA and MPO in the colon, were significantly decreased in the DSS + HRW group compared with the DSS group(P < 0.05). Simultaneously, the protective indicators, superoxide dismutase and glutathione, were markedly increased with the use of HRW. Inflammatory factors were assessed, and the results showed that the DSS + HRW group exhibited significantly reduced levels of TNF-α, IL-6 and IL-1β compared with the DSS group(P < 0.05). In addition, the pivotal proteins involved in endoplasmic reticulum(ER) stress, including p-e IF2α, ATF4, XBP1 s and CHOP, were dramatically reduced after HRW treatment in contrast to the control group(P < 0.05). Furthermore, HRW treatment markedly up-regulated HO-1 expression, and the use of Zn PP obviously reversed the protective role of HRW. In the DSS + HRW + ZnP P group, colon shortening and colonic wall thickening were significantly aggravated, and the macroscopic damage scores were similar to those of the DSS + HRW group(P < 0.05). The histological study also showed more serious colonic damage that was similar to the DSS group.CONCLUSION HRW has a significant therapeutic potential in IBD by inhibiting inflammatory factors, oxidative stress and ER stress and by up-regulating HO-1 expression. 展开更多
关键词 Hydrogen Inflammatory bowel disease Oxidative stress Endoplasmic reticulum stress Heme oxygenase-1
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Inhibiting heme oxygenase-1 attenuates rat liver fibrosis by removing iron accumulation 认领 引用 被引量：18
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作者 Qiu-Ming Wang Jian-Ling Du +3 位作者 Zhi-Jun Duan Shi-Bin Guo Xiao-Yu Sun Zhen Liu 《World Journal of Gastroenterology》 SCIE CAS 2013年第19期2921-2934,共14页
AIM:To investigate the effects of the heme oxygenase(HO)-1/carbon monoxide system on iron deposition and portal pressure in rats with hepatic fibrosis induced by bile duct ligation(BDL).METHODS:Male Sprague-Dawley rat... AIM:To investigate the effects of the heme oxygenase(HO)-1/carbon monoxide system on iron deposition and portal pressure in rats with hepatic fibrosis induced by bile duct ligation(BDL).METHODS:Male Sprague-Dawley rats were divided randomly into a Sham group,BDL group,Fe group,deferoxamine(DFX) group,zinc protoporphyrin(ZnPP) group and cobalt protoporphyrin(CoPP) group.The levels of HO-1 were detected using different methods.The serum carboxyhemoglobin(COHb),iron,and portal vein pressure(PVP) were also quantified.The plasma and mRNA levels of hepcidin were measured.Hepatic fibrosis and its main pathway were assessed using Van Gieson's stain,hydroxyproline,transforming growth factor-β1(TGF-β1),nuclear factor-E2-related factor 2(Nrf2),matrix metalloproteinase-2(MMP-2) and tissue inhibitor of metalloproteinase-1(TIMP-1).RESULTS:Serum COHb and protein and mRNA expression levels of HO-1 and Nrf2 were increased in the BDL group compared with the Sham group and were much higher in the CoPP group.The ZnPP group showed lower expression of HO-1 and Nrf2 and lower COHb.The levels of iron and PVP were enhanced in the BDL group but were lower in the ZnPP and DFX groups and were higher in the CoPP and Fe groups.Hepcidin levels were higher,whereas superoxide dismutase levels were increased and malonaldehyde levels were decreased in the ZnPP and DFX groups.The ZnPP group also showed inhibited TGF-β1 expression and regulated TIMP-1/MMP-2 expression,as well as obviously attenuated liver fibrosis.CONCLUSION:Reducing hepatic iron deposition and CO levels by inhibiting HO-1 activity though the Nrf2/Keap pathway could be helpful in improving hepatic fibrosis and regulating PVP. 展开更多
关键词 Heme oxygenase-1 Hepcidin Iron accumulation Oxidative stress Portal vein pressure Carboxyhemoglobin Bile duct ligation
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Heme oxygenase-1 protects rat liver against warm ischemia/reperfusion injury via TLR2/TLR4-triggered signaling pathways 认领 引用 被引量：13
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作者 Han-Fei Huang Zhong Zeng +6 位作者 Kun-Hua Wang Hai-Yan Zhang Shuai Wang Wen-Xiang Zhou Zhan-Bo Wang Wang-Gang Xu Jian Duan 《World Journal of Gastroenterology》 SCIE CAS 2015年第10期2937-2948,共12页
AIM:To investigate the efficacy and molecularmechanisms of induced heme oxygenase(HO)-1 in protecting liver from warm ischemiaeperfusion(I/R)injury.METHODS:Partial warm ischemia was produced in the left and middle hep... AIM:To investigate the efficacy and molecularmechanisms of induced heme oxygenase(HO)-1 in protecting liver from warm ischemiaeperfusion(I/R)injury.METHODS:Partial warm ischemia was produced in the left and middle hepatic lobes of SD rats for 75min,followed by 6 h of reperfusion.Rats were treated with saline,cobalt protoporphyrin(Co PP)or zinc protoporphyrin(Zn PP)at 24 h prior to the ischemia insult.Blood and samples of ischemic lobes subjected to ischemia were collected at 6 h after reperfusion.Serum transaminases level,plasma lactate dehydrogenase and myeloperoxidase activity in liver were measured.Liver histological injury and inflammatory cell infiltration were evaluated by tissue section and liver immunohistochemical analysis.We used quantitative reverse transcription polymerase chain reaction to analyze liver expression of inflammatory cytokines and chemokines.The cell lysates were subjected to immunoprecipitation with anti-Toll-IL-1R-containing adaptor inducing interferon-β(TRIF)and anti-myeloid differentiation factor 88(My D88),and then the immunoprecipitates were analyzed by SDS-PAGE and immunoblotted with the indicated antibodies.RESULTS:HO-1 protected livers from I/R injury,as evidenced by diminished liver enzymes and wellpreserved tissue architecture.In comparison with Zn PP livers 6 h after surgery,Co PP treatment livers showed a significant increase inflammatory cell infiltration of lymphocytes,plasma cells,neutrophils and macrophages.The Toll-like receptor(TLR)-4 and TANK binding kinase1 protein levels of rats treated with Co PP significantly reduced in TRIF-immunoprecipitated complex,as compared with Zn PP treatment.In addition,pretreatment with Co PP reduced the expression levels of TLR2,TLR4,IL-1R-associated kinase(IRAK)-1 and tumor necrosis factor receptor-associated factor 6 in My D88-immunoprecipitated complex.The inflammatory cytokines and chemokines m RNA expression rapidly decreased inCo PP-pretreated liver,compared with the Zn PP-treated group.However,the expression of negative regulators Tollinteracting protein,suppressor of cytokine signaling-1,IRAK-M and Src homology 2 domain-containing inositol-5-phosphatase-1 in Co PP treatment rats were markedly up-regulated as compared with Zn PP-treated rats.CONCLUSION:HO-1 protects liver against I/R injury by inhibiting TLR2/TLR4-triggered My D88-and TRIFdependent signaling pathways and increasing expression of negative regulators of TLR signaling in rats. 展开更多
关键词 Heme oxygenase-1 Ischemia reperfusion injury Toll-
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Heme oxygenase-1 prevents liver fibrosis in rats by regulating the expression of PPAR_γ and NF-_κB 认领 引用 被引量：20
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作者 Hui Yang Long-Feng Zhao +3 位作者 Zhong-Fu Zhao Yan Wang Jing-Jing Zhao Li Zhang 《World Journal of Gastroenterology》 SCIE CAS CSCD 2012年第14期1680-1688,共9页
AIM:To investigate the effects of heme oxygenase(HO)-1 on liver fibrosis and the expression of peroxisome proliferator-activated receptor gamma(PPARγ) and nuclear factor-kappa B(NF-κB) in rats.METHODS:Sixty Wistar r... AIM:To investigate the effects of heme oxygenase(HO)-1 on liver fibrosis and the expression of peroxisome proliferator-activated receptor gamma(PPARγ) and nuclear factor-kappa B(NF-κB) in rats.METHODS:Sixty Wistar rats were used to construct liver fibrosis models and were randomly divided into 5 groups:group A(normal,untreated),group B(model for 4 wk,untreated),group C(model for 6 wk,untreated),group D [model for 6 wk,treated with zinc protoporphyrin Ⅸ(ZnPP-Ⅸ) from week 4 to week 6],group E(model for 6 wk,treated with hemin from week 4 to week 6).Next,liver injury was assessed by measuring serum alanine aminotransferase(ALT),aspartate aminotransferase(AST) and albumin levels.The degree of hepatic fibrosis was evaluated by measuring serum hyaluronate acid(HA),type Ⅳ collagen(Ⅳ-C) and by histological examination.Hydroxyproline(Hyp) content in the liver homogenate was determined.The expres-sion levels of alpha-smooth muscle actin(α-SMA) in liver tissue were measured by real-time quantitative polymerase chain reaction(RT-PCR).The expression levels of PPARγ and NF-κB were determined by RT-PCR and Western blotting.RESULTS:The expression of HO-1 increased with the development of fibrosis.Induction of HO-1 by hemin significantly attenuated the severity of liver injury and the levels of liver fibrosis as compared with inhibition of HO-1 by ZnPP-Ⅸ.The concentrations of serum ALT,AST,HA and Ⅳ-C in group E decreased compared with group C and group D(P < 0.01).Amount of Hyp and α-SMA in the liver tissues in group E decreased compared with group C(0.62 ± 0.14 vs 0.84 ± 0.07,1.42 ± 0.17 vs 1.84 ± 0.17,respectively,P < 0.01) and group D(0.62 ± 0.14 vs 1.11 ± 0.16,1.42 ± 0.17 vs 2.56 ± 0.37,respectively,P < 0.01).The expression of PPARγ at levels of transcription and translation decreased with the development of fibrosis especially in group D;and it increased in group E compared with groups C and D(0.88 ± 0.15 vs 0.56 ± 0.19,0.88 ± 0.15 vs 0.41 ± 0.11,respectively,P < 0.01).The expression of NF-κB increased with the development of fibrosis especially in group D;and it decreased in group E compared with groups C and D(1.43 ± 0.31 vs 1.89 ± 0.29,1.43 ± 0.31 vs 2.53 ± 0.54,respectively,P < 0.01).CONCLUSION:Our data demonstrate a potential mechanism that HO-1 can prevent liver fibrosis by enhancing the expression of PPARγ and decreasing the expression of NF-κB in liver tissues. 展开更多
关键词 Heme oxygenase-1 Peroxisome proliferator-activated receptor gamma Nuclear factor-kappa B Liver fibrosis Hemin
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Heme oxygenase-1 and gut ischemia/reperfusion injury: A short review 认领 引用 被引量：15
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作者 Yu-Feng Liao Wei Zhu +1 位作者 Dong-Pei Li Xiao Zhu 《World Journal of Gastroenterology》 SCIE CAS 2013年第23期3555-3561,共7页
Ischemiaeperfusion (I/R) injury of the gut is a significant problem in a variety of clinical settings and is associated with a high morbidity and mortality. Although the mechanisms involved in the pathogenesis of gut ... Ischemiaeperfusion (I/R) injury of the gut is a significant problem in a variety of clinical settings and is associated with a high morbidity and mortality. Although the mechanisms involved in the pathogenesis of gut I/R injury have not been fully elucidated, it is generally believed that oxidative stress with subsequent inflammatory injury plays an important role. Heme oxygenase (HO) is the rate-limiting enzyme in the catabolism of heme, followed by production of CO, biliverdin, and free iron. The HO system is believed to confer cytoprotection by inhibiting inflammation, oxidation, and apoptosis, and maintaining microcirculation. HO-1, an inducible form of HO, serves a vital metabolic function as the rate-limiting step in the heme degradation pathway, and affords protection in models of intestinal I/R injury. HO-1 system is an important player in intestinal I/R injury condition, and may offer new targets for the management of this condition. 展开更多
关键词 Heme oxygenase Ischemiaeperfusion injury Oxidative stress Cytoprotection Gut
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Adeno-associated virus-mediated heme oxygenase-1 gene transfer suppresses the progression of micronodular cirrhosis in rats 认领 引用 被引量：9
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作者 Tung-Yu Tsui Chi-Keung Lau +4 位作者 Jian Ma Gabriel Glockzin Aiman Obed Hans J Schlitt Sheung-Tat Fan 《World Journal of Gastroenterology》 SCIE CAS 2006年第13期2016-2023,共8页
AIM： To test the hypothesis that enhancement of the activity of heine oxygenase can interfere with processes of fibrogenesis associated with recurrent liver injury, we investigated the therapeutic potential of over-e... AIM： To test the hypothesis that enhancement of the activity of heine oxygenase can interfere with processes of fibrogenesis associated with recurrent liver injury, we investigated the therapeutic potential of over-expression of heine oxygense-1 in a CCl4-induced micronodular cirrhosis model. METHODS： Recombinant adeno-associated viruses carrying rat HO-1 or GFP gene were generated, 1×10^12 vg of adeno-associated viruses were administered through portal injection at the time of the induction of liver fibrosis. RESULTS： Conditioning the rat liver with over-expression of HO-1 by rAAV/HO-1 significantly increased the HO enzymatic activities in a stable manner. The development of micronodular cirrhosis was significantly inhibited in rAAV/HO-1-transduced animals as compared to controls. Portal hypertension was markedly diminished in rAAV/HO-1-transduced animals as compared to controls, whereas there are no significant changes in systolic blood pressure. This finding was accompanied with improved liver biochemistry, less infiltrating macrophages and less activated hepatic stellate cells （HSCs） in rAAV/ HO-1-transduced livers. CONCLUSIONS： Enhancement of HO activity in the livers suppresses the development of cirrhosis. 展开更多
关键词 Cirrhosis Portal hypertension Heme oxygenase Gene therapy Adeno-associated virus
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