人参皂苷Rb_1减轻阿霉素诱导心肌细胞自噬的保护作用  

Protective effect of ginsenoside Rb_1 on doxorubicin-induced myocardial autophagy

作　　者：李龙飞[1] 马增春[1] 王宇光[1] 汤响林[1] 谭洪玲[1] 肖成荣[1] 高月[1] 

机构地区：[1]军事医学科学院放射与辐射医学研究所,北京100850

出　　处：《中国中药杂志》2017年第7期1365-1369,共5页China Journal of Chinese Materia Medica

基　　金：国家自然科学基金项目(81630102;81673633)

摘　　要：该研究以H9c2细胞为研究对象,采用阿霉素诱导心肌细胞自噬活化,探讨人参皂苷Rb_1对阿霉素诱导心肌细胞自噬的作用。应用CCK-8法、透射电镜观察、荧光染色观察、Western blot等方法分别检测药物作用后H9c2细胞的增殖以及自噬变化。结果显示,阿霉素引起H9c2细胞活力下降,导致H9c2细胞的自噬相关结构增加、自噬标志性蛋白LC3由LC3-I转变为LC3-Ⅱ增加及p62蛋白表达降低;人参皂苷Rb_1可以减弱阿霉素引起的心肌细胞活力下降并抑制阿霉素诱导的自噬相关结构增加、LC3-I转变为LC3-Ⅱ的增加以及p62蛋白表达的降低。以上结果提示,阿霉素可引起H9c2细胞死亡并诱导细胞自噬的活化,而人参皂苷Rb_1对阿霉素诱导心肌细胞死亡具有保护作用,这种作用可能是通过调节自噬产生的。Ginsenoside Rb1（Rb1）, which is one of the main ingredients derived from Panax ginseng, has been found to have extensive pharmacological activities including antioxidant, anti-inflammatory, anticancer properties. In this study, the effect of Rb1 on doxorubicin-induced myocardial autophagy was studied with H9c2 as the study object. CCK-8 method, transmission electron microscope observation, fluorescence staining observation and Western blot were used to detect changes in H9c2 cell proliferation and autophagy after treatment. According to the results, doxorubicin could cause cell viability decrease, significant increase in the LC3-Ⅱ/LC3-I ratio and down-regulation of the expression of p62. Pretreatment with ginsenoside Rb1 inhibited cell viability decrease and increase in doxorubicin-induced autophagic structure and LC3-Ⅱ/LC3-I ratio, and down-regulation of the expression of p62. In conclusion, doxorubicin could induce H9c2 cell death and induce autophagy, and ginsenoside Rb1 showed a protective effect on DOX-induced cardiotoxicity, which may be correlated with suppression of DOX-induced autophagy.

关 键 词：人参皂苷RB1 阿霉素 自噬 H9C2细胞 

分 类 号：R285[医药卫生—中药学]