详细信息
SREBP-1C、GRP-94在小鼠肝细胞脂质代谢中的作用 被引量:4
Role of SREBP-1C and GRP-94 in hepatocytes lipids metabolism of mice
文献类型:期刊文献
中文题名:SREBP-1C、GRP-94在小鼠肝细胞脂质代谢中的作用
英文题名:Role of SREBP-1C and GRP-94 in hepatocytes lipids metabolism of mice
作者:黄丹文[1];晏春根[1];朱东方[1];倪培华[2]
机构:[1]绍兴文理学院医学院附属医院;[2]上海交通大学医学院检验系
年份:2007
卷号:27
期号:5
起止页码:509
中文期刊名:基础医学与临床
外文期刊名:Basic & Clinical Medicine
收录:CSTPCD、、北大核心2004、CSCD2011_2012、北大核心、CSCD
基金:浙江省教育规划课题(20041234)
语种:中文
中文关键词:固醇调节元件结合蛋白1C;葡萄糖调节蛋白94;同型半胱氨酸;脂质代谢;肝细胞
外文关键词:sterol regulatory element binding protein 1C; glucose-regulated protein 94 ; Homocysteine; Lipids Metabolize; Hepatocytes
中文摘要:目的探讨高同型半胱氨酸(Hcy)血症中肝细胞固醇调节元件结合蛋白(SREBP-1C)与葡萄糖调节蛋白94(GRP-94)的表达变化,评价内质网应激蛋白对肝细胞脂质代谢的影响。方法高蛋氨酸饮食诱导小鼠高Hcy血症,分析肝细胞内甘油三酯(TGE)、胆固醇(CHO)含量的变化,RT-PCR、Western blot分别检测内质网应激蛋白SREBP-1C和GRP-94mRNA及其蛋白表达。结果高蛋氨酸饮食后小鼠各时点血浆Hcy及肝细胞内TGE、CHO含量均显著升高,而血浆TGE、CHO含量升高并不明显;小鼠肝细胞内质网应激蛋白SREBP-1C和GRP-94mRNA及其蛋白表达也显著升高(P<0·05)。结论Hcy诱导的内质网应激可引起SREBP-1C、GRP-94的表达变化及内源性固醇调节通路失调。
外文摘要:Objective To explore the expression of sterol regulatory dement binding protein 1C ( SREBP-1 C) and glucose-regulated protein 94 (GRP-94) in hyperhomocysteinmia and to evaluate the effects of endoplasmic reticulum stress proteins on hepatocytes lipids metabolism. Methods After hyperhomocysteinmia C57BL/6 mice model being induced by high methionine diet, TGE and CHO of Hepatocytes were determined, and the expression of SREBP-1C and GRP-94 was assessed by RT-PCR and Western blot. All data were compared to those in control group's. Results The level of plasmic homocysteine (Hcy) and hepatocytes TGE or CHO of high methlonine diet mice at different time point significantly ascended(P 〈0. 05 compared with 0 week). But plasmic TGE and CHO level had no change. The expressions of rnRNAs and proteins of GRP-94 and SREBP-1C at different time point after high methionine diet were higher than that of at 0 week (P 〈 0. 05 ). Conclusion Hcy-induced endoplasmic reticulum stress causes the expression change of SREBP-1C and GRP-94, the dysregulation of the endogenous sterol response pathway.
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