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Neuroprotection mediated by the Wnt/Frizzled signaling pathway in early brain injury induced by subarachnoid hemorrhage 预览
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作者 Yang Wang De-Jun Bao +4 位作者 Bin Xu Chuan-Dong Cheng Yong-Fei Dong Xiang-pin Wei Chao-Shi Niu 《中国神经再生研究:英文版》 SCIE CAS CSCD 2019年第6期1013-1024,共12页
The Wnt/Frizzled signaling pathway participates in many inflammation-linked diseases.However,the inflammatory response mediated by the Wnt/Frizzled signaling pathway in experimental subarachnoid hemorrhage has not bee... The Wnt/Frizzled signaling pathway participates in many inflammation-linked diseases.However,the inflammatory response mediated by the Wnt/Frizzled signaling pathway in experimental subarachnoid hemorrhage has not been thoroughly investigated.Consequently,in this study,we examined the potential role of the Wnt/Frizzled signaling pathway in early brain injury in rat models of subarachnoid hemorrhage.Simultaneously,possible neuroprotective mechanisms were also investigated.Experimental subarachnoid hemorrhage rat models were induced by injecting autologous blood into the prechiasmatic cistern.Experiment 1 was designed to examine expression of the Wnt/Frizzled signaling pathway in early brain injury induced by subarachnoid hemorrhage.In total,42 adult rats were divided into sham(injection of equivalent volume of saline),6-,12-,24-,48-,72-hour,and 1-week subarachnoid hemorrhage groups.Experiment 2 was designed to examine neuroprotective mechanisms of the Wnt/Frizzled signaling pathway in early brain injury induced by subarachnoid hemorrhage.Rats were treated with recombinant human Wnt1(rhwnt1),small interfering Wnt1(siwnt1)RNA,and monoclonal antibody of Frizzled1(anti-Frizzled1)at 48 hours after subarachnoid hemorrhage.Expression levels of Wnt1,Frizzled1,β-catenin,peroxisome proliferator-activated receptor-γ,CD36,and active nuclear factor-κB were examined by western blot assay and immunofluorescence staining.Microglia type conversion and inflammatory cytokine levels in brain tissue were examined by immunofluorescence staining and enzyme-linked immunosorbent assay.Our results show that compared with the sham group,expression levels of Wnt1,Frizzled1,andβ-catenin were low and reduced to a minimum at 48 hours,gradually returning to baseline at 1 week after subarachnoid hemorrhage.rhwnt1 treatment markedly increased Wnt1 expression and alleviated subarachnoid hemorrhage-induced early brain injury(within 72 hours),including cortical cell apoptosis,brain edema,and neurobehavioral deficits,accompanied by increasing prot 展开更多
关键词 nerve REGENERATION SUBARACHNOID hemorrhage Wnt/Frizzled signaling pathway early brain injury nuclear factor-κB M2 type MICROGLIA PEROXISOME proliferator-activated receptor-γ inflammatory cytokines neural REGENERATION
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鱼类脂肪酸β-氧化研究进展 预览
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作者 宁丽军 李加敏 +1 位作者 孙胜香 杜震宇 《水产学报》 CAS CSCD 北大核心 2019年第1期128-142,共15页
脂肪酸β-氧化是动物脂肪酸分解代谢的主要途径,在动物生理活动的能量供应和代谢内稳态的维持方面具有举足轻重的作用。在哺乳动物中,关于脂肪酸β-氧化的研究已有大量报道,但是在鱼类中,脂肪酸β-氧化研究相对较少。随着水产养殖业对... 脂肪酸β-氧化是动物脂肪酸分解代谢的主要途径,在动物生理活动的能量供应和代谢内稳态的维持方面具有举足轻重的作用。在哺乳动物中,关于脂肪酸β-氧化的研究已有大量报道,但是在鱼类中,脂肪酸β-氧化研究相对较少。随着水产养殖业对提高饲料脂肪分解供能和降低鱼体脂肪的要求日益迫切,鱼类脂肪酸β-氧化反应及其组成和调控体系越来越受到学界和产业界的关注。为此,本文从鱼类脂肪酸β-氧化体系组成和关键酶系、β-氧化的组织和底物特异性、β-氧化体系调控因子以及鱼类脂肪酸β-氧化的影响因素等几个方面全面综述了鱼类脂肪酸β-氧化的研究进展,并比较了鱼类脂肪酸β-氧化反应及其组成和调控体系在鱼类与哺乳动物之间,乃至不同鱼种之间的异同,以期为人们更深入地理解鱼类脂代谢与调控体系并开展相关应用研究提供有价值的参考资料。 展开更多
关键词 鱼类 脂肪酸β-氧化 线粒体 过氧化物酶体 能量 代谢调控
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Anti-Hypertensive Action of Fenofibrate via UCP2 Upregulation Mediated by PPAR Activation in Baroreflex Afferent Pathway
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作者 Jian Guan Miao Zhao +8 位作者 Chao He Xue Li Ying Li Jie Sun Wei Wang Ya-Li Cui Qing Zhang Bai-Yan Li Guo-Fen Qiao 《神经科学通报:英文版》 SCIE CAS CSCD 2019年第1期15-24,共10页
Fenofibrate, an agonist for peroxisome proliferator-activated receptor alpha(PPAR-a), lowers blood pressure, but whether this action is mediated via baroreflex afferents has not been elucidated. In this study, the dis... Fenofibrate, an agonist for peroxisome proliferator-activated receptor alpha(PPAR-a), lowers blood pressure, but whether this action is mediated via baroreflex afferents has not been elucidated. In this study, the distribution of PPAR-a and PPAR-c was assessed in the nodose ganglion(NG) and the nucleus of the solitary tract(NTS). Hypertension induced by drinking high fructose(HFD) was reduced, along with complete restoration of impaired baroreceptor sensitivity, by chronic treatment with fenofibrate. The molecular data also showed that both PPAR-a and PPAR-c were dramatically up-regulated in the NG and NTS of the HFD group. Expression of the downstream signaling molecule of PPAR-a, the mitochondrial uncoupling protein 2(UCP2), was up-regulated in the baroreflex afferent pathway under similar experimental conditions, along with amelioration of reduced superoxide dismutase activity and increased superoxide in HFD rats.These results suggest that chronic treatment with fenofibrate plays a crucial role in the neural control of blood pressure by improving baroreflex afferent function due at least partially to PPAR-mediated up-regulation of UCP2 expression and reduction of oxidative stress. 展开更多
关键词 FENOFIBRATE PEROXISOME proliferator-activated receptor Mitochondrial UNCOUPLING protein BAROREFLEX AFFERENT function Blood pressure regulation
Crosstalk between gut microbiota and antidiabetic drug action 预览
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作者 Yevheniia Kyriachenko Tetyana Falalyeyeva +2 位作者 Oleksandr Korotkyi Nataliia Molochek Nazarii Kobyliak 《世界糖尿病杂志:英文版(电子版)》 2019年第3期154-168,共15页
Type 2 diabetes (T2D) is a disorder characterized by chronic inflated blood glucose levels (hyperglycemia), at first due to insulin resistance and unregulated insulin secretion but with tendency towards global spreadi... Type 2 diabetes (T2D) is a disorder characterized by chronic inflated blood glucose levels (hyperglycemia), at first due to insulin resistance and unregulated insulin secretion but with tendency towards global spreading. The gut microbiota is recognized to have an influence on T2D, although surveys have not formed a clear overview to date. Because of the interactions between gut microbiota and host homeostasis, intestinal bacteria are believed to play a large role in various diseases, including metabolic syndrome, obesity and associated disease. In this review, we highlight the animal and human studies which have elucidated the roles of metformin,α-glucosidase inhibitors, glucagon-like peptide-1 agonists, peroxisome proliferator-activated receptors γ agonists, inhibitors of dipeptidyl peptidase-4, sodium/glucose cotransporter inhibitors, and other less studied medications on gut microbiota. This review is dedicated to one of the most widespread diseases, T2D, and the currently used antidiabetic drugs and most promising new findings. In general, the gut microbiota has been shown to have an influence on host metabolism, food consumption, satiety, glucose homoeostasis, and weight gain. Altered intestinal microbiota composition has been noticed in cardiovascular diseases, colon cancer, rheumatoid arthritis, T2D, and obesity. Therefore, the main effect of antidiabetic drugs is on the microbiome composition, basically increasing the short-chain fatty acids-producing bacteria, responsible for losing weight and suppressing inflammation. 展开更多
关键词 Type 2 diabetes Gut microbiota Metformin Α-GLUCOSIDASE INHIBITORS Glucagon-like peptide-1 AGONISTS PEROXISOME proliferator-activated receptors γ AGONISTS Dipeptidyl peptidase-4 INHIBITORS Sodium/glucose COTRANSPORTER INHIBITORS
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Effects of Mitochondrial Dysfunction via AMPK/PGC-1α Signal Pathway on Pathogenic Mechanism of Diabetic Peripheral Neuropathy and the Protective Effects of Chinese Medicine
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作者 ZHANG Qian LIANG Xiao-chun 《中国结合医学杂志:英文版》 SCIE CAS CSCD 2019年第5期386-394,共9页
Diabetic peripheral neuropathy(DPN) is a progressive neurodegenerative disease of peripheral nervous system with high energy requirement. The adenosine monophosphate-activated protein kinase(AMPK)/peroxisome prolifera... Diabetic peripheral neuropathy(DPN) is a progressive neurodegenerative disease of peripheral nervous system with high energy requirement. The adenosine monophosphate-activated protein kinase(AMPK)/peroxisome proliferator-activated receptor-γ coactivator 1α(PGC-1α) axis plays a key role in regulating mitochondrial energy metabolism. Increasing preclinical evidences have shown that inhibition of AMPK/PGC-1α pathway leading to mitochondrial dysfunction in neurons or Schwann cells contributes to neuron apoptosis, distal axonopathy and nerve demyelination in DPN. Some Chinese medicine formulae or extracts from herbs may have potential neuroprotective effects on DPN via activating AMPK/PGC-1α pathway and improving mitochondrial function. 展开更多
关键词 monophosphate-activated protein kinase PEROXISOME proliferator-activated receptor-γ COACTIVATOR SIRTUINS diabetic peripheral neuropathy Chinese medicine
Hepatitis C virus core protein modulates several signaling pathways involved in hepatocellular carcinoma 预览
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作者 Shahab Mahmoudvand Somayeh Shokri +1 位作者 Reza Taherkhani Fatemeh Farshadpour 《世界胃肠病学杂志:英文版》 SCIE CAS 2019年第1期42-58,共17页
Hepatocellular carcinoma(HCC)is the fifth most common cancer,and hepatitis C virus(HCV)infection plays a major role in HCC development.The molecular mechanisms by which HCV infection leads to HCC are varied.HCV core p... Hepatocellular carcinoma(HCC)is the fifth most common cancer,and hepatitis C virus(HCV)infection plays a major role in HCC development.The molecular mechanisms by which HCV infection leads to HCC are varied.HCV core protein is an important risk factor in HCV-associated liver pathogenesis and can modulate several signaling pathways involved in cell cycle regulation,cell growth promotion,cell proliferation,apoptosis,oxidative stress and lipid metabolism.The dysregulation of signaling pathways such as transforming growth factorβ(TGF-β),vascular endothelial growth factor(VEGF),Wnt/β-catenin(WNT),cyclooxygenase-2(COX-2)and peroxisome proliferator-activated receptorα(PPARα)by HCV core protein is implicated in the development of HCC.Therefore,it has been suggested that this protein be considered a favorable target for further studies in the development of HCC.In addition,considering the axial role of these signaling pathways in HCC,they are considered druggable targets for cancer therapy.Therefore,using strategies to limit the dysregulation effects of core protein on these signaling pathways seems necessary to prevent HCV-related HCC. 展开更多
关键词 Hepatitis C virus Core protein TRANSFORMING GROWTH factorβ Vascular endothelial GROWTH FACTOR WNT/Β-CATENIN CYCLOOXYGENASE-2 PEROXISOME proliferatoractivated receptorα Hepatocellular carcinoma
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Metabolic and hepatic effects of liraglutide,obeticholic acid and elafibranor in diet-induced obese mouse models of biopsy-confirmed nonalcoholic steatohepatitis 预览
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作者 Kirstine S Tolbol Maria NB Kristiansen +6 位作者 Henrik H Hansen Sanne S Veidal Kristoffer TG Rigbolt Matthew P Gillum Jacob Jelsing Niels Vrang Michael Feigh 《世界胃肠病学杂志:英文版》 SCIE CAS 2018年第2期179-194,共16页
AIM To evaluate the pharmacodynamics of compounds in clinical development for nonalcoholic steatohepatitis(NASH)in obese mouse models of biopsy-confirmed NASH.METHODS Male wild-type C57BL/6J mice(DIO-NASH)and Lepob/ob... AIM To evaluate the pharmacodynamics of compounds in clinical development for nonalcoholic steatohepatitis(NASH)in obese mouse models of biopsy-confirmed NASH.METHODS Male wild-type C57BL/6J mice(DIO-NASH)and Lepob/ob(ob/ob-NASH)mice were fed a diet high in trans-fat(40%),fructose(20%)and cholesterol(2%)for 30 and 21 wk,respectively.Prior to treatment,all mice underwent liver biopsy for confirmation and stratification of liver steatosis and fibrosis,using the nonalcoholic fatty liver disease activity score(NAS)and fibrosis staging system.The mice were kept on the diet and received vehicle,liraglutide(0.2 mg/kg,SC,BID),obeticholic acid(OCA,30 mg/kg PO,QD),or elafibranor(30 mg/kg PO,QD)for eight weeks.Within-subject comparisons were performed on changes in steatosis,inflammation,ballooning degeneration,and fibrosis scores.In addition,compound effects were evaluated by quantitative liver histology,including percent fractional area of liver fat,galectin-3,and collagen 1a1.RESULTS Liraglutide and elafibranor,but not OCA,reduced body weight in both models.Liraglutide improved steatosis scores in DIO-NASH mice only.Elafibranor and OCA reduced histopathological scores of hepatic steatosis and inflammation in both models,but only elafibranor reduced fibrosis severity.Liraglutide and OCA reduced total liver fat,collagen 1a1,and galectin-3 content,driven by significant reductions in liver weight.The individual drug effects on NASH histological endpoints were supported by global gene expression(RNA sequencing)and liver lipid biochemistry.CONCLUSION DIO-NASH and ob/ob-NASH mouse models show distinct treatment effects of liraglutide,OCA,and elafibranor,being in general agreement with corresponding findings in clinical trials for NASH.The present data therefore further supports the clinical translatability and utility of DIO-NASH and ob/ob-NASH mouse models of NASH for probing the therapeutic efficacy of compounds in preclinical drug development for NASH. 展开更多
关键词 Nonalcoholic steatohepatitis Disease models Pathology Fibrosis Liver BIOPSY TRANSCRIPTOMICS PHARMACODYNAMICS Glucagon-like peptide-1 RECEPTOR PEROXISOME proliferator-activated RECEPTOR Farnesoid X RECEPTOR
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多器官功能障碍综合征患者外周血单个核细胞内PPARγ和COX-2的关系 预览
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作者 徐飞 乔万海 《陕西医学杂志》 CAS 2018年第9期1105-1108,共4页
目的:探讨多器官功能障碍综合征(MODS)患者外周血单个核细胞(PBMC)中PPARγ与COX-2的关系。方法:收集MODS患者60例(分为三组各20例,MODS1组APACHEⅡ评分0~10分,MODS 2组11~20分,MODS 3组评分>20分及正常对照组(20例健康对照者)。确... 目的:探讨多器官功能障碍综合征(MODS)患者外周血单个核细胞(PBMC)中PPARγ与COX-2的关系。方法:收集MODS患者60例(分为三组各20例,MODS1组APACHEⅡ评分0~10分,MODS 2组11~20分,MODS 3组评分>20分及正常对照组(20例健康对照者)。确诊后分别于1d、3d、6d取静脉血,采用逆转录聚合酶链反应检测PPARγ、COX-2的表达与同期健康对照组进行比较分析。结果:①正常组PBMC s中PPARγ、COX-2表达量均较少。与正常组比较,MODS1组PPARγ、COX-2表达均明显增高,随治疗时间推移,PPARγ表达明显增高(P<0.05),而COX-2的表达则明显降低(P<0.05)。MODS2组、MODS3组PPARγ的表达低于正常对照组,随着治疗时间的增加,PPARγ明显下降(P<0.05);COX-2的表达高于正常对照组,随着治疗时间的增加,COX-2明显升高(P<0.05)。②相关结果分析表明:PBMCs中PPARγ与COX-2的表达在MODS1组,MODS2组,MODS3组呈负相关性(MODS1组:P<0.01;MODS2组:P<0.01;MODS3组:P<0.01,在正常对照组无明显相关性(P>0.05)。结论:PPARγ可能通过抑制COX-2的表达对MODS患者起到保护作用,为PPARγ内源性配体用于临床MODS的防治提供依据。 展开更多
关键词 多器官功能衰竭/病理生理学 过氧化物酶体增殖物激活受体γ/分析 环氧合酶2/分析 单核细胞
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circRNA_0046366 inhibits hepatocellular steatosis by normalization of PPAR signaling 预览
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作者 Xing-Ya Guo Fang Sun +3 位作者 Jian-Neng Chen Yu-Qin Wang Qin Pan Jian-Gao Fan 《世界胃肠病学杂志:英文版》 SCIE CAS 2018年第3期323-337,共15页
AIM To investigate micro(mi)R-34a-antagonizing circular(circ)RNA that underlies hepatocellular steatosis.METHODS The effect of circRNA on miR-34a was recognized by the miRNA response element(MRE),and validated by the ... AIM To investigate micro(mi)R-34a-antagonizing circular(circ)RNA that underlies hepatocellular steatosis.METHODS The effect of circRNA on miR-34a was recognized by the miRNA response element(MRE),and validated by the dual-luciferase reporter assay.Its association with hepatocellular steatosis was investigated in HepG2-based hepatocellular steatosis induced by free fatty acids(FFAs;2:1 oleate:palmitate)stimulation.After normalization of the steatosis-related circRNA by expression vector,analysis of miR-34a activity,peroxisome proliferator-activated receptor(PPAR)αlevel,and expression of downstream genes were carried out so as to reveal its impact on the miR-34a/PPARαregulatory system.Both triglyceride(TG)assessment and cytopathological manifestations uncovered the role of circRNA in miR-34a-dependent hepatosteatogenesis.RESULTS Bioinformatic and functional analysis verified circRNA_0046366 to antagonize the activity of miR-34a via MRE-based complementation.In contrast to its lowered level during FFA-induced hepatocellular steatosis,circRNA_0046366 up-regulation abolished the miR-34a-dependent inhibition of PPARαthat played a critical role in metabolic signaling pathways.PPARαrestoration exerted transcriptional improvement to multiple genes responsible for lipid metabolism.TGspecific lipolytic genes[carnitine palmitoyltransferase 1A(CPT1A)and solute-carrier family 27A(SLC27A)]among these showed significant increase in their expression levels.The circRNA_0046366-related rebalancing of lipid homeostasis led to dramatic reduction of TG content,and resulted in the ameliorated phenotype of hepatocellular steatosis.CONCLUSION Dysregulation of circRNA_0046366/miR-34a/PPARαsignaling may be a novel epigenetic mechanism underlying hepatocellular steatosis.circRNA_0046366 serves as a potential target for the treatment of hepatic steatosis. 展开更多
关键词 HEPATOCYTES STEATOSIS circRNA_0046366 MIR-34A PEROXISOME proliferator-activated receptorα
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Chronic oleoylethanolamide treatment attenuates diabetes-induced mice encephalopathyby activating peroxisome proliferator-activatedreceptor alpha in hippocampus
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作者 REN Tong LIU Jin-feng +11 位作者 ZHUO Ren-gong XU Lan-xi ZHANG Yi-jiao ZHANG Hui-jun PENG Lu CHEN Cai-xia ZHOU Yu ZHAO Yun LI Wen-jun LI Ying JIN Xin YANG Li-chao 《中国药理学与毒理学杂志》 CSCD 北大核心 2018年第9期680-681,共2页
OBJECTIVE Oleoylethanolamide (OEA) is an endogenous peroxisome proliferatoractivated receptor alpha (PPARα) agonist that acts on the peripheral control of energy metabolism. Previous studies have shown that OEA exert... OBJECTIVE Oleoylethanolamide (OEA) is an endogenous peroxisome proliferatoractivated receptor alpha (PPARα) agonist that acts on the peripheral control of energy metabolism. Previous studies have shown that OEA exerts neuroprotection after cerebral ischemia. However, whether OEA affects the outcomes of diabetes-induced encephalopathy (DE) requires further study. METHODS The chronic effects of OEA on DE were evaluated in C57BL / 6 and PPARα knockout mice, individually. The cognitive function was assessed with Morris water maze. The expression of receptor for advanced glycation end products (RAGE) and phosphorylation of Tau in mice hippocampus were determined using Western blotting. The influence of OEA in neuron loss and neuroplasticity were assessed with immunofluorescent staining and Western blotting. RESULTS OEA markedly ameliorated performance in the Morris water maze, which was correlated with its capabilities of suppressing glycometabolism and phosphorylation of Tau in the hippocampus. OEA offered protection from diabetes-induced impairments in hippocampal neu-roplasticity. Furthermore, the changes in Morris water maze performance and neuron loss could not be observed in PPARα knockout mouse models with OEA administration. CONCLUSION The ability of OEA to control PPARα signaling can serve as a novel neuroprotective approach for the treatment of diabetes-induced encepha-lopathy. 展开更多
关键词 OLEOYLETHANOLAMIDE diabeticencephalopathy spatial cognitive function NEUROPROTECTION PEROXISOME proliferator-activated receptor ALPHA
Mutual interaction between oxidative stress and endoplasmic reticulum stress in the pathogenesis of diseases specifically focusing on non-alcoholic fatty liver disease 预览
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作者 Junichi Fujii Takujiro Homma +1 位作者 Sho Kobayashi Han Geuk Seo 《世界生物化学杂志:英文版(电子版)》 2018年第1期1-15,共15页
Reactive oxygen species(ROS)are produced during normal physiologic processes with the consumption of oxygen.While ROS play signaling roles,when they are produced in excess beyond normal antioxidative capacity this can... Reactive oxygen species(ROS)are produced during normal physiologic processes with the consumption of oxygen.While ROS play signaling roles,when they are produced in excess beyond normal antioxidative capacity this can cause pathogenic damage to cells.The majority of such oxidation occurs in polyunsaturated fatty acids and sulfhydryl group in proteins,resulting in lipid peroxidation and protein misfolding,respectively.The accumulation of misfolded proteins in the endoplasmic reticulum(ER)is enhanced under conditions of oxidative stress and results in ER stress,which,together,leads to the malfunction of cellular homeostasis.Multiple types of defensive machinery are activated in unfolded protein response under ER stress to resolve this unfavorable situation.ER stress triggers the malfunction of protein secretion and is associated with a variety of pathogenic conditions including defective insulin secretion from pancreaticβ-cells and accelerated lipid droplet formation in hepatocytes.Herein we use nonalcoholic fatty liver disease(NAFLD)as an illustration of such pathological liver conditions that result from ER stress in association with oxidative stress.Protecting the ER by eliminating excessive ROS via the administration of antioxidants or by enhancing lipidmetabolizing capacity via the activation of peroxisome proliferator-activated receptors represent promising therapeutics for NAFLD. 展开更多
关键词 Oxidative STRESS Reactive oxygen species Endoplasmic reticulum STRESS NONALCOHOLIC FATTY liver disease PEROXISOME proliferator-activated receptor
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活性氧对鼠早期胚胎抗氧化酶基因表达的影响 被引量:1
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作者 井洋洋 方南洙 +3 位作者 张宝修 胡德宝 赵丽娟 李钟淑 《中国兽医学报》 CAS CSCD 北大核心 2017年第2期335-344,共10页
通过检测鼠早期胚胎内过氧化物酶体数量及过氧化物酶体中抗氧化酶基因表达水平,以探讨活性氧对鼠胚胎2-细胞期过氧化物酶体数量的变化及过氧化物酶体中抗氧化酶基因表达量的影响。结果表明:MmSOD、GPX-1和GPX-4目的基因在鼠胚胎4-细... 通过检测鼠早期胚胎内过氧化物酶体数量及过氧化物酶体中抗氧化酶基因表达水平,以探讨活性氧对鼠胚胎2-细胞期过氧化物酶体数量的变化及过氧化物酶体中抗氧化酶基因表达量的影响。结果表明:MmSOD、GPX-1和GPX-4目的基因在鼠胚胎4-细胞期表达量最高;CAT和GPX-2目的基因在卵母细胞表达量最高;Cu/Zn-SOD目的基因在2-细胞期表达量最高;GPX3目的基因在卵母细胞、1-细胞、2-细胞和4-细胞期间表达无明显差异。H2O2处理组中PMP-20、Cu/Zn-SOD、Mn-SOD和GPX-3基因表达量较高,GPX-2基N表达量较低,而GPX-4基因在体外培养组中表达量最高,GPX-1基因表达量无显著变化,CAT基因没有表达。由此可知,不同抗氧化酶基因表达量在鼠早期胚胎发育的不同时期有所不同,Mn-SOD、GPX-1和GPX-4基因表达量随着胚胎的发育不断增高,而过氧化物酶体数量同时也随之增加。 展开更多
关键词 活性氧 小鼠 胚胎 抗氧化酶 过氧化物酶体
谷胱甘肽硫转移酶K1研究进展 预览
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作者 胡纯 孙林 《中南大学学报:医学版》 CSCD 北大核心 2017年第4期468-475,共8页
谷胱甘肽硫转移酶K1(glutathione S-transferase kappa 1,GSTK1)是一个参与脂联素分泌和多聚化的关键蛋白,且在线虫中已经证实,GSTK1与能量产生和脂质代谢有关。同时GSTK1表达水平与肥胖呈负相关,并能缓解内质网应激诱导的脂联素水平... 谷胱甘肽硫转移酶K1(glutathione S-transferase kappa 1,GSTK1)是一个参与脂联素分泌和多聚化的关键蛋白,且在线虫中已经证实,GSTK1与能量产生和脂质代谢有关。同时GSTK1表达水平与肥胖呈负相关,并能缓解内质网应激诱导的脂联素水平下降,而且人GSTK1启动子的多态性与胰岛素分泌和脂肪沉积有关,因此,GSTK1可能成为一个治疗胰岛素抵抗及其相关的代谢疾病潜在的药物新靶点。 展开更多
关键词 谷胱甘肽硫转移酶K1 线粒体 过氧化物酶体 脂联素
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过氧化物酶体增殖剂对稻瘟病菌生长发育及致病性的影响
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作者 陈海莉 李玲 +2 位作者 王教瑜 张昕 孙国昌 《微生物学报》 CAS CSCD 北大核心 2016年第10期1606-1615,共10页
【目的】探索过氧化物酶体增殖剂(Peroxisome proliferators,PPs)对稻瘟病菌生长发育及致病性的影响。【方法】在6种不同的PPs诱导下,观察比较稻瘟病菌过氧化物酶体数量及相关基因表达、生长速率、孢子萌发、附着胞形成与致病性的差... 【目的】探索过氧化物酶体增殖剂(Peroxisome proliferators,PPs)对稻瘟病菌生长发育及致病性的影响。【方法】在6种不同的PPs诱导下,观察比较稻瘟病菌过氧化物酶体数量及相关基因表达、生长速率、孢子萌发、附着胞形成与致病性的差异。【结果】在不同的PPs诱导下,稻瘟病菌过氧化物酶体数量均呈现明显的增加,同时过氧化物酶体形成相关基因PEX8、PEX11、PEX14的表达量升高;PPs影响病菌菌丝生长、分生孢子萌发及附着孢形成,并导致致病性的减弱。其中,2,4-D与阿司匹林的抑制效果最为显著。同时,2,4-D与ASA对稻瘟病菌过氧化物酶体形成突变体Δpex5和Δpex7的生长抑制效果与野生菌株相比明显增加。【结论】首次将PPs类化合物用于模式丝状病原真菌稻瘟病菌的研究。研究发现6种PPs均能够引起过氧化物酶体的增殖,并可抑制稻瘟病菌生长发育,降低致病性。 展开更多
关键词 稻瘟病菌 过氧化物酶体 PPS PEX基因
Psoriasis treatment:Unconventional and non-standard modalities in the era of biologics 预览 被引量:1
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作者 Vikram K Mahajan 《世界皮肤病学杂志》 2016年第1期17-51,共35页
Psoriasis is a potentially debilitating inflammatory dermatosis affecting 0.2%-4.8%of the population worldwide causing a significant occupational,personal or psychosocial morbidity to these patients for life.The basic... Psoriasis is a potentially debilitating inflammatory dermatosis affecting 0.2%-4.8%of the population worldwide causing a significant occupational,personal or psychosocial morbidity to these patients for life.The basic aim of psoriasis therapy is to control the disease to maximum possible extent and improve the patient’s quality of life.Management of triggers for flareups,lifestyle modifications,and dietary supplements are often recommended.Intermittent or rotational therapy with frequent alterations in treatment options is usually needed to reduce toxicity of anti-psoriatic drugs in the absence of safer alternatives.Currently,several biological agents categorized as either T-cell targeted(e.g.,Alefacept,Efalizumab)or cytokine modulating(e.g.,Adalimumab,Infliximab,Etanercept)are available for treating severe psoriasis.However,their high cost is often precluding for most patients.The usefulness of systemic(methotrexate,cyclosporine,acitretin or several other therapeutic agents)or topical(tar,anthralin,corticosteroids or calcipotriol ointments,phototherapy with or without psoralens)therapies has been well established for the management of psoriasis.The literature is also replete with benefits of less used non-standard and unconventional treatment modalities(hydroxycarbamide,azathioprine,leflunomide,mycophenolate mofetil,isotretinoin,fumarates,topical calcineurin inhibitors,peroxisome proliferator-activated receptors agonists,statins,sulfasalazine,pentoxifylline,colchicine,grenz ray therapy,excimer laser,climatotherapy and balneophototherapy,peritoneal dialysis,tonsillectomy,ichthyotherapy,etc.).These can be used alternatively to treat psoriasis patients who have mild/minimal lesions,are intolerant to conventional drugs,have developed side effects or achieved recommended cumulative dose,where comorbidities pose unusual therapeutic challenges,or may be as intermittent,rotational or combination treatment alternatives. 展开更多
关键词 Acetretin Azathioprine Balneophototherapy Calcineurin inhibitors CALCIPOTRIOL Calcium dobesilate Climatotherapy Colchicine Cyclosporine DAPSONE Excimer laser Fumarates Grenz ray therapy Hydroxycarbamide Ichthyotherapy ISOTRETINOIN Leflunamide Methotrexate MYCOPHENOLATE mofetil Pentoxifylline Peritoneal dialysis Phototherpy Plaque PSORIASIS Peroxisome proliferator-activated receptors agonists Statins SULFASALAZINE Tonsillectomy
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玉米大斑病菌StPEX11基因家族的鉴定及生物信息学分析
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作者 马兰 薛韶娜 +5 位作者 冯胜泽 赵洁 巩校东 谷守芹 韩建民 董金皋 《玉米科学》 CAS CSCD 北大核心 2016年第6期36-40,共5页
PEX11基因家族成员是参与过氧化物酶体增殖调控的关键因子。在玉米大斑病菌基因组中鉴定出2个PEX11基因,根据其相对分子质量分别命名为StPEX11-1和StPEX11-2。利用生物信息学方法,对基因结构、蛋白质的保守结构域及理化性质进行分析,预... PEX11基因家族成员是参与过氧化物酶体增殖调控的关键因子。在玉米大斑病菌基因组中鉴定出2个PEX11基因,根据其相对分子质量分别命名为StPEX11-1和StPEX11-2。利用生物信息学方法,对基因结构、蛋白质的保守结构域及理化性质进行分析,预测其二级结构域。系统发育树分析发现,玉米大斑病菌的2个StPEX11基因分别属于I型和III型的PEX11亚家族。 展开更多
关键词 玉米 玉米大斑病菌 StPEX11基因家族 过氧化物酶体
Crosstalk between mitochondria and peroxisomes 预览
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作者 Jean Demarquoy Fran?oise Le Borgne 《世界生物化学杂志:英文版(电子版)》 2015年第4期301-309,共9页
Mitochondria and peroxisomes are small ubiquitous organelles. They both play major roles in cell metabolism,especially in terms of fatty acid metabolism,reactive oxygen species(ROS) production,and ROS scavenging,and i... Mitochondria and peroxisomes are small ubiquitous organelles. They both play major roles in cell metabolism,especially in terms of fatty acid metabolism,reactive oxygen species(ROS) production,and ROS scavenging,and it is now clear that they metabolically interact with each other. These two organelles share some properties,such as great plasticity and high potency to adapt their form and number according to cell requirements. Their functions are connected,and any alteration in the function of mitochondria may induce changes inperoxisomal physiology. The objective of this paper was to highlight the interconnection and the crosstalk existing between mitochondria and peroxisomes. Special emphasis was placed on the best known connections between these organelles:origin,structure,and metabolic interconnections. 展开更多
关键词 PEROXISOME MITOCHONDRION Beta-oxidation REACTIVE o
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溶酶体与过氧化物酶体形成膜接触介导胆固醇转运 被引量:1
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作者 褚贝贝 宋保亮 《中国细胞生物学学报》 CAS CSCD 2015年第6期759-763,共5页
胆固醇是真核细胞中含量非常丰富的一类脂质小分子,其主要生物学功能是掺入到磷脂双分子层中,调节膜的性质。胆固醇在细胞内不同膜上的分布极不均匀而且高度动态运输,这对维持细胞的正常生命活动至关重要。然而,细胞内胆固醇运输的机制... 胆固醇是真核细胞中含量非常丰富的一类脂质小分子,其主要生物学功能是掺入到磷脂双分子层中,调节膜的性质。胆固醇在细胞内不同膜上的分布极不均匀而且高度动态运输,这对维持细胞的正常生命活动至关重要。然而,细胞内胆固醇运输的机制一直不清楚。针对这一胆固醇代谢领域的重要问题,同时也是一个基本的细胞生物学问题,通过巧妙设计、全基因组筛选,鉴定出341个参与细胞内胆固醇转运的候选基因,其中,过氧化物酶体相关基因被显著富集。进而发现溶酶体通过和过氧化物酶体相互接触,将胆固醇转移给后者。而介导该接触的分子分别是溶酶体上的Synaptotagmin VII(Syt7)和过氧化物酶体膜上的PI(4,5)P2磷脂。将这种新发现的溶酶体–过氧化物酶体膜接触命名为LPMC(lysosome-peroxisome membrane contacts)。过氧化物酶体功能缺失会导致一大类相关疾病—过氧化物酶体紊乱疾病,表现为发育和神经系统功能障碍,目前还没有有效的治疗手段。该工作第一次揭示在这些病人和小鼠模型的细胞中有大量胆固醇堆积,且该现象的出现大大早于神经症状,提示胆固醇堆积是过氧化物酶体紊乱疾病的发病原因之一。这项研究工作的意义在于:(1)发现了细胞内胆固醇运输的新途径;(2)揭示了过氧化物酶体这一细胞器的新功能;(3)证明胆固醇运输异常是导致过氧化物酶体紊乱疾病的病因之一,为治疗该类疾病提供了全新的思路。 展开更多
关键词 胆固醇 溶酶体 过氧化物酶体 Syt7 PI(4 5)P2
Selective silencing of 2Cys and type-IIB Peroxiredoxins discloses their roles in cell redox state and stress signaling
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作者 Patricia Vidigal Ana Montserrat Martin-Hernandez +2 位作者 Celia Guiu-Aragones Sara Amancio Luisa Carvalho 《植物学报:英文版》 SCIE CAS CSCD 2015年第6期591-601,共11页
Peroxiredoxins (Prx ) catalyse 氢过氧化物的减小(H <sub>2</sub > O <sub>2</sub>) 并且与过氧化氢酶和另外的 peroxidases 联合,可以由调整细胞间的 H <sub>2</sub 参予信号 transduction > ... Peroxiredoxins (Prx ) catalyse 氢过氧化物的减小(H <sub>2</sub > O <sub>2</sub>) 并且与过氧化氢酶和另外的 peroxidases 联合,可以由调整细胞间的 H <sub>2</sub 参予信号 transduction > 能接着控制基因抄写并且房间发信号的 O <sub>2</sub> 集中。用 virus-induced-gene-silencing ( VIGS ), 2-Cys Peroxiredoxin ( 2CysPrx )家庭和 type-II Peroxiredoxin B ( PrxIIB )基因是在 Nicotiana benthamiana 的 silenced ,为了学习每 Prx 的功能的损失将在控制( 22 &thinsp;&deg;C )和严重的热下面在抗氧化剂系统有的影响,强调条件( 48 &thinsp;&deg;C )。结果两个都显示出那 Prxs 在不同细胞器,影响 ascorbate 的新生到重要程度,但是与不同目的。2CysPrx 影响 abscisic 酸(骆驼毛的织物) 通过 ascorbate 的生合成,当 PrxIIB 通过黄色色素可能做它时,骑车。而且, 2CysPrx 在 H <sub>2</sub 是关键的 > 清除并且反应的氧种类和 PrxIIB 下游地在在骆驼毛的织物的规定的后果发信号的 O <sub>2</sub> 为 H <sub>2</sub 提供重要帮助 > O <sub>2</sub> peroxisome 清除。 展开更多
关键词 细胞信号转导 氧化还原状态 力信号 过氧化物酶体 过氧化氢酶 H2O2 B型 控制基因
生酮饮食对难治性癫痫患儿 Th 细胞亚群的影响 被引量:5
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作者 崔萍萍 李成荣 +4 位作者 李秋 廖建湘 王国兵 林素芳 陈黎 《中华微生物学和免疫学杂志》 CAS CSCD 北大核心 2015年第3期225-231,共7页
目的:探讨生酮饮食(ketogenic diet,KD)治疗对难治性癫痫(intractable epilepsy,IP)患儿Th细胞亚群的影响。方法 IP患儿35例,同年龄健康对照组18例。采用流式细胞术分别检测外周血CD3+CD8-IFN-γ+(Th1)细胞、CD3+CD8-IL-... 目的:探讨生酮饮食(ketogenic diet,KD)治疗对难治性癫痫(intractable epilepsy,IP)患儿Th细胞亚群的影响。方法 IP患儿35例,同年龄健康对照组18例。采用流式细胞术分别检测外周血CD3+CD8-IFN-γ+(Th1)细胞、CD3+CD8-IL-17A+(Th17)细胞及CD4+CD25+Foxp3+(Treg)细胞比例;实时荧光定量PCR(real-time PCR)检测外周血CD4+CD25-T细胞中T-bet、ROR-γt、IFN-γ、IL-17A、过氧化物酶增殖物激活受体γ(peroxisome proliferator-activated receptorγ,PPAR-γ)mRNA及CD4+CD25+T细胞Foxp3、GITR、CTLA-4、PPAR-γmRNA的表达;酶联免疫吸附试验( ELISA)检测受试者血浆中前列腺素F2a (prostaglandin F2a,PGF2a)、环氧化酶-2(cyclooxygenases-2,COX-2)蛋白浓度;流式微球阵列技术(CBA)检测受试者血浆IL-17A、IFN-γ蛋白表达水平。结果(1)IP患儿外周血Treg细胞比例明显低于同年龄健康对照组(P<0.05),KD治疗后,Treg细胞数量明显增加(P<0.05);IP患儿外周血Th1、Th17细胞比例明显高于同年龄健康对照组(P<0.05),KD治疗后显著下降(P<0.05);IP患儿外周血CD4+CD25+Treg细胞转录因子Foxp3及相关因子GITR、CTLA-4基因转录水平明显低于健康对照组(P<0.05),治疗后明显上调;CD4+CD25-T细胞中T-bet、ROR-γt、IL-17A、IFN-γ等Th1/Th17细胞相关因子表达量显著高于健康对照组( P<0.05),治疗后明显下降;(2) IP患儿CD4+CD25+及CD4+CD25-细胞PPAR-γ基因表达明显低于对照组(P<0.05),KD治疗后表达量明显上升(P<0.05),相关性分析发现Treg细胞与PPAR-γ表达呈正相关(r=0.61,P<0.05),Th1及Th17细胞与PPAR-γ表达呈负相关[Th1(r=-0.54,P<0.05);Th17(r=-0.64,P<0.05)];(3)IP患儿IL-17A及IFN-γ血浆浓度明显高于健康对照组(P<0.05),KD治疗后明显下降(P<0.05)� 展开更多
关键词 生酮饮食 难治性癫痫 TH细胞亚群 过氧化物酶增殖物激活受体Γ 氧化应激 PEROXISOME proliferator-activated re-ceptorγ
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