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青藤碱抑制H2O2诱导乳鼠心肌细胞凋亡
引用本文:李乐,高小利,丁宝兴.青藤碱抑制H2O2诱导乳鼠心肌细胞凋亡[J].中国中药杂志,2008,33(8):939-942.
作者姓名:李乐  高小利  丁宝兴
摘    要:目的:探讨青藤碱对H2O2诱导乳鼠心肌细胞凋亡的影响及其可能的作用机制.方法:在原代培养的SD大鼠乳鼠心肌细胞上建立H2O2损伤模型,观察不同剂量青藤碱(10,30,100 μmol·L-1)对心肌细胞凋亡率、丙二醛(MDA)含量、超氧化物歧化酶(SOD)活性、乳酸脱氢酶(LDH)活性及NF-KB蛋白表达的影响.结果:H2O2组与空白对照组相比,心肌细胞凋亡率显著增加(P<0.01),并随着时间的延长其凋亡率不断增高;青藤碱明显抑制H2O2所诱导各个时问段的心肌细胞凋亡率(P<0. 01),降低MDA含量,增加SOD,LDH活性,抑制NF-KB蛋白表达.结论:青藤碱对H2O2诱导的乳鼠心肌细胞凋亡有抑制作用,其作用机制可能与其抗脂质氧化、抑制心肌细胞表达NF-KB有关.

关 键 词:青藤碱  过氧化氢  心肌细胞  凋亡  青藤碱  乳鼠心肌细胞  心肌细胞凋亡  cardiomyocytes  neonatal  rat  apoptosis  sinomenine  effect  细胞表达  抗脂质氧化  抑制作用  细胞凋亡率  延长  时间  对照组  结果  蛋白表达  乳酸脱氢酶  活性  超氧化物歧化酶
文章编号:1001-5302(2008)08-0939-04
修稿时间:2007年12月12

Inhibitory effect of sinomenine on H2O2-induced apoptosis in neonatal rat cardiomyocytes
LI Le,GAO Xiao-li,DING Bao-xin.Inhibitory effect of sinomenine on H2O2-induced apoptosis in neonatal rat cardiomyocytes[J].China Journal of Chinese Materia Medica,2008,33(8):939-942.
Authors:LI Le  GAO Xiao-li  DING Bao-xin
Institution:School of Pharmacy, Zhejiang University of Technology, Hangzhou 310014, China. lile_1856@163.com
Abstract:OBJECTIVE: To study the effects of sinomenine on apoptosis in cutured neonatal rat cardiomyocytes induced by H2O2 and its possible mechanism. METHOD: H2O2 was used to build an oxidative stress-induced injury model in neonatal rat cardiomyocytes after being treated with sinomenine (10, 30, 100 micromol L(-1)), the apoptosis rate, the content of malondialdehyde (MDA), the activity of superoxide dimutase (SOD), the activity of lactate dehydrogenase (LDH) and expression of NF-kappaB protein of the Cardiomyocytes were examined. RESULT: Compared with the model group, the apoptosis rate and the content of MDA, LDH decreased greatly (P < 0.01), and the activity of SOD increased distinctly (P < 0.01) after being treated by sinomenine (10, 30, 100 micromol x L(-1)). CONCLUSION: Sinomenine can inhibit the apoptosis induced by H2O2 in neonatal rat cardiomyocytes. The protective mechanism could be related to its ability to reduce lipid pexosidation and to inhibit cardiomyocyte expression of NF-kappaB protein.
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