摘要
目的探讨氯离子通道阻断剂DIDS(4,4′-diisothiocy-ano-2,2′-stilbene-disulfonic acid)对staurosporine(STS)诱导心肌细胞凋亡的调节蛋白Bcl-2/Bax表达的影响。方法在STS诱导心肌细胞凋亡模型上,观察DIDS对心肌细胞存活率、caspase-3活性、Bcl-2/Bax蛋白表达水平及Bax细胞内分布的影响。实验分组:对照组、STS组、DIDS组。结果与STS组比较,DIDS能够明显抑制STS诱导的心肌细胞凋亡发生,心肌细胞存活率增加,caspase-3活性水平降低(P<0.01)。对照组、STS组和DIDS组在全细胞水平上Bcl-2、Bax表达差异无显著性(P>0.01),在亚细胞水平上发现STS组有明显的Bax蛋白从胞质向线粒体转位,DIDS可以抑制STS诱导的Bax线粒体转位。结论DIDS抑制心肌细胞凋亡可能与抑制促凋亡分子Bax由胞质向线粒体转位有关。
Aim To explore effects of chloride channel blocker DIDS on Bcl-2/Bax expressions in STS-induced cardiomyocyte apoptosis. Methods Primary cultured neonatal rat cardiomyocytes were exposed to STS to induce apoptosis;the effect of DIDS on the cell viability, caspase-3 activity, Bcl-2/Bax expressions and Bax intra^cellular distribution were observed. The experiment included a control group, a STS group and a DIDS group. Results DIDS exerted a significant antiapoptotic effect on STS-induced cardiomyocytes with an increased cell viability and decreased caspase-3 activity （P 〈 0.01 vs STS ）. No significances were found in Bcl-2 and Bax expression among the control group,STS group and DIDS group at cellular level（ P 〉 0.01 ）. Ex-posure of cells to STS resulted in Bax translocation from cytoplasm to mitochondria and DIDS effectively inhibited STS-induced Bax transiocation to mitochondria. Conclusion DIDS can significantly protect cardio- myocytes against STS-induced apoptosis and the cyto- protective effect may be inter related with the inhibition of Bax translocation from cytoplasm to mitochondria.
出处
《中国药理学通报》
CAS
CSCD
北大核心
2009年第1期47-50,共4页
Chinese Pharmacological Bulletin
基金
国家自然科学基金资助课题(No30570758,30770847)
作者简介
刘安恒（1978-），男，博士，主治医师，研究方向：心血管内科学，E-mail：cloctorlah@126．com；
王晓明（1965-），男，博士，副教授，副主任医师，硕士生导师，研究方向：心血管疾病的基础与临床，通讯作者，Tel：029—84775543，E-mail：xmwang@fmmu．edu．cn
