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慢性氧化应激诱导兔动脉粥样硬化对蛋白酶体26S及20S活性影响的实验研究

Laboratory study on the proteasome 26S and 20S activity alteration in atherosclerosis induced by chronic oxidative stress

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【作者】 谭春江谭宁锋陈文列沈双宏蔡晶杜建李玉光

【Author】 TAN Chun-jiang*,TAN Ning-feng,CHEN Wen-lie,et al.*Institute of Traditional and Western Medicine,Fujian University of TCM,Fuzhou 350018,China

【机构】 福建中医学院中西医结合研究院湖南省新田县人民医院汕头大学医学院

【摘要】 目的探讨慢性氧化应激诱导动脉粥样硬化(AS)对蛋白酶体26S及20S活性的影响,以及与泛素/泛素蛋白结合物(Ub/UPC)表达之间的关系。方法新西兰雄性兔30只,随机分为正常饮食组(N)和高胆固醇饮食组(H),共饲养12周。检测26S及20S的活性,观察腹主动脉的病理变化、Ub/UPC的表达及氧化应激等指标。结果成功诱导了AS模型,H组的20S的活性比N组明显增高(P<0.01),而26S的活性两组间差异无统计学意义(P>0.05),Ub/UPC在H组的表达比N组明显增强。结论慢性氧化应激状态下,20S的活性明显增强,Ub/UPC大量聚集,可能在AS的病理变化过程中起着重要的作用。

【Abstract】 Objective To investigate correlation of proteasome 26S and 20S alteration in atherosclerosis and the accumulation of ubiquitin/ubiquitin-conjugates induced by chronic oxidized stress.Methods 30 New Zealand rabbits were randomized into normal diet (N) or therogenic diet (H) for 12 weeks.Proteasome activity,pathologic changes and ubiquitin/ubiquitin-conjugates(ub/upc) were investigated by Western blotting or immuno-chemistry.Results Atherosclerosis models were successfully induced by chronic oxidative stress.20S activity was significantly higher in H vs N(P<0.01),no significant difference of 26S activity was noted between two groups(P> 0.05).ub/upc was significantly increased H vs N.Conclusion Excessive activity of 20S and accumulation of ub/ upc may play an active role in the pathogenesis of AS induced by chronic oxidadive stress.

【基金】 福建省高校中西医结合基础重点实验室开放课题(ZXY2008005);陈可冀中西医结合发展基金(CKZ2008009);福建省自然科学基金(2008J0326)
  • 【文献出处】 中国心血管病研究 ,Chinese Journal of Cardiovascular Review , 编辑部邮箱 ,2008年11期
  • 【分类号】R543
  • 【被引频次】9
  • 【下载频次】167
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