摘要
目的观察黄酮类化合物包括高良姜素(G)、山萘酚(K)、芹菜素(A)、桑色素(M)、槲皮素(Q)、杨梅素(MY)对H2O2诱导的心肌细胞凋亡的作用,并探讨其可能的作用机制。方法培养新生Wistar乳鼠心肌细胞,随机分为正常组、模型组、药物组。分别用荧光染色法、琼脂糖凝胶电泳法、Western blot法观察心肌细胞凋亡情况及蛋白表达的变化。结果100μmol·L-1H2O2孵育心肌细胞16 h能明显诱导心肌细胞凋亡(P<0.01),黄酮类化合物能降低细胞凋亡率,抑制DNA损伤,上调bcl-2、bcl-xl,下调bax蛋白表达。结论黄酮类化合物能抗氧化,从而抑制心肌细胞凋亡,主要是通过线粒体死亡途径调节bcl-2家族蛋白表达来发挥作用的。
Aim To observe the effects of flavonoids, including galangin （G）, kaempferol （ K ）, apigenin （A） ,morin（M） ,quercetin （Q） and myricetin（MY） , on myocardial apoptosis induced by Hz02, and explore the possible mechanism. Methods Primary cultured cardiocytes of neonatal rat were randomly divided into normal group, model group, and flavonoids group. Fluorescent staining, electrophoresis and Western-blot were employed to observe the cardiocyte apoptosis and proteins expression. Results Exposure to 100 μmol · L^-1 H2O2 for 16 h resulted in myocardial apoptosis significantly （ P 〈 0. 01 ）, preincubation with the fla-vonoids could decrease the rate of apoptosis, protect myocardial cells against H202-induced DNA damage and up-regulate bcl-2, bcl-xl, down-regulate bax pro- tein expression. Conclusion Flavonoids have an ap- parent higher potential for decreasing the cardiocyte apoptosis in relation to their antioxidant activity, their an- tiapoptotic effects are probably mediated by regulating bcl-2 family proteins expression through mitochondrial death pathway.
出处
《中国药理学通报》
CAS
CSCD
北大核心
2008年第5期635-639,共5页
Chinese Pharmacological Bulletin
基金
国家自然科学基金资助项目(No30371684)
黑龙江省自然科学基金资助项目(NoD0301)
