>
网站首页期刊介绍通知公告编 委 会投稿须知电子期刊广告合作联系我们
最新消息:
丹参酮ⅡA对高糖培养的大鼠血管平滑肌细胞p38MAPK信号通路的影响
作者:陆璐 李新荣 邓湘蕾 
单位:东南大学,发育与疾病相关基因实验室,江苏,南京,210009
关键词:丹参酮ⅡA 高糖 血管平滑肌细胞 氧化应激 丝裂原活化蛋白激酶p38 
分类号:R587.1, R-33
出版年·卷·期(页码):2008·27·第二期(130-133)
摘要:

目的:观察丹参酮ⅡA对高糖诱导的血管平滑肌细胞增殖的影响,分析该作用与氧化应激以及丝裂原活化蛋白激酶p38(p38 mitogen-activated protein kinases,p38 MAPK)信号通路的关系.方法:取第3代原代培养的大鼠血管平滑肌细胞建立高糖诱导细胞增殖模型,实验分为正常对照组、高糖组和丹参酮ⅡA组,BrdU掺入法测定血管平滑肌细胞的DNA合成水平;黄嘌呤氧化酶法、硫代巴比妥酸法分别测定细胞培养上清中超氧化物歧化酶(SOD)、丙二醛(MDA)含量;免疫印迹法(Western blot)检测磷酸化p38MAPK蛋白表达.结果:高糖诱导的血管平滑肌细胞呈快速增殖状态,在10~25 mmol·L-1间增殖效应呈剂量依赖性;丹参酮ⅡA能抑制高糖诱导的血管平滑肌细胞增殖,提高高糖培养的细胞中SOD水平,降低MDA含量,减少p-p38MAPK蛋白的表达.结论:丹参酮ⅡA抑制高糖诱导的血管平滑肌细胞增殖,这可能与其能减少血管平滑肌细胞中的氧自由基,抑制p38MAPK信号通路有关.

Objective To observe the effect of tanshinone ⅡA(TSN) on proliferation of vascular smooth muscle cell(VSMC) induced by high glucose and explore its relationship with oxidative stress and p38MAPK signal transduction pathway.Methods The arterial blood vessels of rats were separated carefully to culture VSMC by the tissue adherence method,and the third generation cells were employed for experiment.The cells were divided into normal control group,high glucose group and TSN group.DNA synthesis was analyzed by ELISA of BrdU.The activity of SOD and the contents of MDA in medium were measured with Xanthine oxidase method and TBA method.The expression levels of phosphorylated p38MAPK were detected by Western blot.Results The proliferation of VSMC induced by high glucose appeared fast,and the effect was in a dose-dependent manner in a concentration range of 10-25 mmol·L-1.TSN can restrain the proliferation of VSMC under the high glucose.And it also had an effect on the SOD and MDA in medium.The expression levels of phosphorylated p38MAPK of VSMC pretreated with TSN was lower than that of the VSMC stimulated by high glucose.Conclution TSN suppresses the proliferation of VSMC induced by high glucose,which is possiblely related with the suppression of oxygen free radical and p38MAPK signal transduction pathway.

参考文献:

[1] ROSS R. The pathogenesis of atherosclerosis:a perspective for the 1990s. 1993(6423). doi:10.1038/362801a0
[2] 李新荣, 李艳平, 邓湘蕾. 丹参酮ⅡA对大鼠血管平滑肌细胞的增殖作用. 中国临床康复2006(31)
[3] GIANNATTASIO C, MANCIA G. Arterial distensibility in humans.Modulating mechanisms,alterations in diseases and effects of treatment. 2002(10). doi:10.1097/00004872-200210000-00001
[4] TOMLINSON D R. Mitogen-activated protein kinases as glucose transducers for diabetic complications. 1999(11). doi:10.1007/s001250051439
[5] CERIELLO M, MOROCUTTI A, MERCURI F. Defective intracellular antioxidant eazyme production in type 1 diabetic patients with nephropathy. 2000(12). doi:10.2337/diabetes.49.12.2170
[6] TITLE L M, CUMMINGS P M, GIDDENS K. Oral glucose loading acutely attenuates endothelium -dependent vasodilation in healthy adults without diabetes:an effect prevented by vitamins C and E. 2000(7). doi:10.1016/S0735-1097(0)00980-3
[7] WILMER W A, DIXON C L, HEBERT C. Chronic exposure of human mesangial cells to high glucose environments activates p38MAPK pathway. 2001(3). doi:10.1046/j.1523-1755.2001.060003858.x
[8] FONTAYNE A, DANG P M, GOUGEROT-POCIDALO M A. Phosphorylation of p47phox sites by PKC alpha,beta Ⅱ,delta,and zeta:effect on binding to p22phox and on NADPH oxidase activation. 2002(24). doi:10.1021/bi011953s
[9] EVANS J L, GOLDFINE I D, MADDUX B A. Are oxidative stress-activated signaling pathways mediators of insulin resistance and beta-cell dysfunction?. 2003(1). doi:10.2337/diabetes.52.1.1
[10] BEGUM N, RAGOLIA L. High glucose and insulin inhibit VSMC MKP-1 expression by blocking iNOS via p38 MAPK activation, 2000(1)

服务与反馈:
文章下载】【发表评论】【查看评论】【加入收藏
提示:您还未登录,请登录!点此登录
您是第 410685 位访问者


copyright ©《东南大学学报(医学版)》编辑部
联系电话:025-83272481 83272483
电子邮件:
bjb@pub.seu.edu.cn

苏ICP备09058364