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Astaxanthin delayed the pathogenesis of diabetic nephropathy in type 1 diabetic rats

BIOCELL 2022年第8期46卷 1911-1916页

作者： LIANHUAN MA SHOUPENG LIU XIAOWEN ZHEN WEIWEI QIAO LINA MA XIAOMIN ZHANG Department of Diagnostics The Second School of Clinical MedicineBinzhou Medical UniversityYantai264003China School of Public Health and Management Binzhou Medical UniversityYantai264003China Department of Nephrology Binzhou Medical University HospitalBinzhou256603China

This study was designed to investigate the protective effects of Astaxanthin(AST)in rats with diabetes mellitus(DM)induced by *** rats were divided into control group(n=5,only received normal saline),DM group(n=8)and AST+DM group(n=8;AST:50 mg/kg/day).DM rats were induced by intraperitoneal injection of streptozocin(STZ,65 mg/kg).Blood glucose level and body weight were determined at weeks 0,2,4,6 and 8,*** week 8,kidney function was determined,together with expression of P53 and dynamin-related protein-1(Drp1)by Western blot analysis and *** led to increase of body weight in rats with ***+DM group showed a significant decrease in blood glucose level at week 4 compared with DM group(P1 in DM *** addition,AST can effectively reduce the blood glucose in DM rats,and delayed the pathogenesis of diabetic *** delay mediated by AST may be associated with the downregulation of Drp1 and P53.

关键词： Astaxanthin Diabetic nephropathy dynamin-related protein-1 P53 Renal function

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Hepatic stimulator substance resists hepatic ischemia-reperfusion injury by regulating Drp1 translocation and activation

Hepatic stimulator substance resists hepatic ischemia-reperf...

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中国生物化学与分子生物学会第十二届全国会员代表大会暨2018年全国学术会议

作者： Chao Zhang Jing Huang Wei An Department of Cell Biology and Municipal Laboratory of Liver Protection and Regulation of Regeneration Capital Medical University

Ischemia-reperfusion injury(IRI),induced by abnormal mitochondrial fission related apoptosis,is a major concern in liver transplantation *** previous studies have demonstrated that hepatic stimulator substance(HSS) is an antiapoptotic effector and could protect liver from ***,the underlying mechanism remains *** the present study,we report that in vitro and in vivo HSS could regulate mitochondrial fission and hepatocyte apoptosis during liver IRI by orchestrating the translocation and activation of dynamin-related protein 1(Drp1).Using a mouse model of IR-induced liver injury,we found that HSS haploinsufficient(HSS+/-) mice displayed exacerbated liver damage based on their increased serum aminotransferase levels,cell structural destruction,and apoptosis levels compared to the wild type(HSS+/+) *** of HSS markedly increased cyclin-dependent kinase 1(CDK1) and Bax expression,accompanied with elevated p-Drp1 and release of cytochrome *** parallel in vitro studies,we found that HSS could inhibit the expression of CDK1 and that HSS inhibits hepatocytes apoptosis through its suppression of CDK1/cyclin B-mediated phosphorylation at Ser-616 of Drp1,thereby decreasing Drp1 accumulation in mitochondria and Drp1-mediated activation of the mitochondrial fission *** the contrary,knockdown of HSS increased of CDK1 as well as Drp1 phosphorylation and aggravated hepatocellular *** investigation showed that HSS was able to reduce the stability and translation of CDK1 mRNA by modulating the expression of several miRNAs,including miR-410-3 p,miR-490-3 p and miR-582-5 *** data reveal a novel mechanism for HSS in regulating the mitochondrial fission machinery and further suggest that modulation of HSS may provide a therapeutic approach for combating liver damage.

关键词： Hepatic stimulator substance dynamin-related protein-1 mitochondrial fission apoptosis ischemia-reperfusion injury

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