四逆汤预防性给药抗心肌细胞凋亡的作用机制探讨  

Effect of delayed preconditioning induced by Sini decoction on myocardial cell apoptosis and its mitochondrial mechanism

作　　者：刘颖[1] 吴伟康[2] 陈晨[3] 段新芬[2] 

机构地区：[1]广东药学院病理生理教研室,广东广州510224 [2]中山大学中西医研究所,广东广州510080 [3]解放军421医院检验科,广东广州510318

出　　处：《中国中药杂志》2006年第15期1269-1272,共4页China Journal of Chinese Materia Medica

基　　金：国家自然科学基金资助项目(39770936)

摘　　要：目的:探讨四逆汤预防性给药24 h后能否抑制心肌缺血再灌注(MI/R)后心肌细胞凋亡的发生及其可能涉及的线粒体机制。方法:SD大鼠分为正常对照组、假手术组、缺血再灌注组、四逆汤预处理组。缺血再灌注组采用经典大鼠冠脉结扎,缺血1 h,再灌1 h。四逆汤预处理组给予四逆汤灌胃(5 g.kg-1.d-1)连续3 d,末次灌药24h后心肌缺血1 h,再灌1 h。流式细胞仪测定心肌细胞凋亡率,进行细胞色素C及抗凋亡蛋白bcl-xl的Western blot-ting分析并检测caspase-3的活性。结果:四逆汤预处理24 h后可以减少MI/R后心肌细胞凋亡率,减少细胞色素C自线粒体的释放,上调bcl-xl蛋白的表达,抑制caspase-3的活化。结论:四逆汤预防性给药24 h后可以减少MI/R造成的细胞凋亡,其机制可能与抑制细胞凋亡的线粒体信号转导通路有关。Objective： To investigate the mechanism of myocardial cell apoptosis during delayed preconditioning induced by Sini decoction （SND）. Method： SD rats were divide into four groups： control, sham, I/R and SND groups. The rats in I/R group, left anterior descending coronary artery （LAD） was occluded for 1h and reperfused for 1 h. The rats in SND group were pretreated with Sini decoction （5 g·kg^-1·d^-1 ） for three days, the last treatment was pretreated 24 h before the index occlusion. Cell apoptosis was measured by flow cytometry, cytochrome C and bcl-xl were detected by Western blotting and the activity of caspase-3 was detected by assay kit. Result： As compared with I/R group, apoptosis rate of myocardial cell, the release of cytochrome C from mitochondria and the activity of caspase-3 were significantly decreased, and the expression of bcl-xl protein was elevated in SND group. Conclusion： The delayed preconditioning induced by Sini decoction decreased myocardial cell apoptosis. The mechanism may be related to the inhibition of mitochondria signal pathway of apoptosis.

关 键 词：四逆汤 延迟预适应 细胞凋亡 BCL-XL 细胞色素C CASPASE-3 

分 类 号：R285.5[医药卫生—中药学]