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硫化氢对动脉粥样硬化胆固醇代谢的调节作用
引用本文:周红,梁小燕,吴志远,戚晓红.硫化氢对动脉粥样硬化胆固醇代谢的调节作用[J].中国药理学通报,2013,29(8).
作者姓名:周红  梁小燕  吴志远  戚晓红
作者单位:1. 南京医科大学基础医学院,实验教学中心,江苏,南京,210029
2. 南京医科大学基础医学院,病理生理学系,江苏,南京,210029
3. 新加坡国立大学医学院药理学系,新加坡,117597
基金项目:江苏高校优势学科建设工程资助项目,南京医科大学科技发展基金重点项目
摘    要:目的观察H2S对动脉粥样硬化(AS)胆固醇代谢的影响,并探究其作用机制。方法用高脂饲料结合维生素D3的方法建立AS大鼠模型,并给与腹腔注射NaHS 56μmol·kg-1.d-1,持续12周。检测血脂水平及肝胆固醇含量。HepG2细胞给与NaHS 100μmol·L-16 h后,用RT-PCR方法检测羟甲基戊二酰辅酶A还原酶(HMGCoA reductase)和低密度脂蛋白受体(LDLR)mRNA表达。结果 NaHS组血清总胆固醇(TC)、甘油三酯(TG)、高密度脂蛋白胆固醇(HDL-Ch)和低密度脂蛋白胆固醇(LDL-Ch)均较模型组降低,肝胆固醇含量下降。NaHS使HepG2细胞HMGCoA Re-ductase mRNA表达下降,LDLR mRNA表达增加。结论H2S对AS胆固醇代谢具有调节作用,能下调肝HMGCoAReductase,使胆固醇合成下降;上调肝脏LDLR表达,降低血清总胆固醇水平。

关 键 词:硫化氢  动脉粥样硬化  羟甲基戊二酰辅酶A还原酶  低密度脂蛋白受体  胆固醇  胆固醇代谢

Regulatory effect of hydrogen sulfide on cholesterol metabolism in atherosclerosis
ZHOU Hong , LIANG Xiao-yan , WU Zhi-yuan , QI Xiao-hong.Regulatory effect of hydrogen sulfide on cholesterol metabolism in atherosclerosis[J].Chinese Pharmacological Bulletin,2013,29(8).
Authors:ZHOU Hong  LIANG Xiao-yan  WU Zhi-yuan  QI Xiao-hong
Abstract:Aim To investigate the effect of hydrogen sulfide(H2S) on cholesterol metabolism in atherosclerosis(AS).Methods AS rat model was established by high fat diet combined with vitamin D3.The NaHS group was performed intraperitoneal injection with NaHS 56 μmol·kg-1·d-1 for 12 wk.The levels of lipid in blood serum and cholesterol in liver were tested respectively.The mRNA expression of hydroxy-methyl-glutaryl coenzyme A reductase(HMGCoA reductase) and low density lipoprotein receptor(LDLR) were observed by RT-PCR after NaHS 100 μmol·L-1 6 h on HepG2 cells.Results The levles of serum total cholesterol(TC),triglyceride(TG),high density lipoprotein cholesterol(HDL-Ch),low density lipoprotein cholesterol(LDL-Ch)and liver cholesterol content in NaHS group were decreased compared with those in model group.NaHS decreased the mRNA expression of HMGCoA reductase and increased the mRNA express of LDLR in HepG2 cells.Conclusion H2S may decrease cholesterol level mainly via the down-regulation of HMGCoA reductase expression and up-regulation of liver LDLR.
Keywords:hydrogen sulfide  atherosclerosis  HMGCoA reductase  LDL receptor  cholesterol  cholesterol metabolism
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