文章摘要
周 光,施晓雷.肝再生增强因子调控线粒体功能稳态在棕榈酸诱导肝细胞脂毒性细胞模型中的作用[J].南京医科大学学报,2019,(10):1421~1425
肝再生增强因子调控线粒体功能稳态在棕榈酸诱导肝细胞脂毒性细胞模型中的作用
Role of augmenter of liver regeneration in cell model of palmitic acid induced hepatocyte lipotoxicity by mediating regulation of mitochondrial homeostasis
投稿时间:2019-05-23  
DOI:10.7655/NYDXBNS20191003
中文关键词: 线粒体  肝细胞脂毒性细胞模型  肝再生增强因子
英文关键词: mitochondria  cell model of hepatocyte lipotoxicity  augmenter of liver regeneration
基金项目:国家自然科学基金(81872359,81670566);中央高校基本科研业务费专项资金(021414380449)
作者单位
周 光 南京医科大学鼓楼临床医学院(南京鼓楼医院)普外科江苏 南京 210008 
施晓雷 南京医科大学鼓楼临床医学院(南京鼓楼医院)普外科江苏 南京 210008 
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中文摘要:
      目的:研究肝细胞脂毒性细胞模型中线粒体内肝再生增强因子(augmenter of liver regeneration,ALR)与线粒体功能障碍之间的关系。方法:以无脂肪酸的10%牛血清蛋白(bull serum albumin,BSA)处理L?O2细胞为对照(BSA组),0.2 mmol/L棕榈酸(palmitic acid,PA)处理L?O2细胞为脂毒性细胞模型(PA组),并在构建ALR过表达(ALR?OE组)及对照(Vector组)细胞后,分别接受BSA和PA处理,CCK?8法检测细胞活力、乳酸脱氢酶(lactic dehydrogenase,LDH)检测试剂盒检测脂毒性、JC?1染色分析线粒体膜电位、流式凋亡检测分析细胞凋亡,Western bolt检测ALR、Bax、Bcl?2、细胞色素C等蛋白表达水平。结果:与BSA组相比,PA组细胞内脂滴增多、细胞活力下降50%、LDH释放增加13倍,线粒体内ALR表达则明显降低。BSA处理下Vector组和ALR?OE组无明显差异,而PA刺激后ALR?OE组相较于Vector组,细胞活力增加约16%,LDH释放减少约40%,线粒体膜电位增加约18%,细胞色素C释放减少,细胞凋亡减少。结论:ALR参与肝细胞脂毒性的发生,靶向调控ALR可在一定程度上抑制脂毒性的发生。
英文摘要:
      Objective:To study the relationship between mitochondrial augmenter of liver regeneration(ALR)and mitochondrial dysfunction in cell model of hepatocyte lipotoxicity. Methods:The 10% fatty acid?free bull serum albumin treated L?O2 cells were used as the control group(BSA group),and L?O2 cells treated with 0.2 mmol/L palmitic acid(PA)as a cell model of hepatocyte lipotoxicity(PA group). Meanwhile,the ALR overexpression group(ALR?OE group)and the empty vector transfected control cell group(Vector group)were constructed and treated with BSA or PA,respectively. cell viability,lactate dehydrogenase(LDH)release,mitochondrial membrane potential changes,apoptosis and related protein expression levels were detected subsequently. Results:Compared with the BSA group,the intracellular lipid droplet increased,the cell viability decreased by about 50%,and the LDH release increased by 13 times,the expression of ALR in the mitochondria was significantly decreased in the PA group. There were no significant differences between the Vector group and the ALR?OE group under BSA treatment conditions. However,the cell viability increased by about 16%,LDH release is reduced by about 40%,mitochondrial membrane potential is increased by about 18%,cytochrome C release is reduced,and apoptosis decreases in the ALR?OE group compared with the Vector group under PA stimulation. Conclusion:ALR is involved in the onset of hepatocellular lipotoxicity,and targeting the regulation of mitochondrial ALR can inhibit the onset of lipotoxicity to a certain extent.
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