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人参皂苷Rb3对多柔比星诱导心脏毒性的保护作用及其机制
张城炼,许卫攀,蔡振璇
0
(湖北理工学院附属医院·鄂东医疗集团黄石市中心医院心血管内科)
摘要:
【摘要】目的 探究人参皂苷Rb3(GRb3)对多柔比星(DOX)诱导心脏毒性的作用及机制。方法 将30只SD大鼠随机分为3组,分别对照组,DOX组(25 mg/kg),DOX+GRb3组(20 mg/kg);另加入PI3K抑制剂分为DOX+Wortmanin组(1 mg·kg-1·d-1)和DOX+GRb3+Wortmanin组(1 mg·kg-1·d-1 )。将DOX(25 mg/kg)以腹腔注射方式在2周内达到注射次数为6次即可建立心肌毒性损伤模型,并且观察GRb3对DOX所致心肌毒性过程中的作用;使用HE染色观察大鼠心肌病理改变;用ELISA试剂盒检测心肌组织中心肌损伤标志物,炎症因子标志物,氧化应激标志物等水平;用Western blotting检测pPI3K、PI3K、pAKT和AKT的蛋白水平。结果 DOX诱导心肌毒性会导致心肌损伤加剧,炎症和氧化应激反应增加。G-Rb3可改善DOX所致的心脏损伤,主要体现在心肌中胶原积累显著减少,心肌损伤标志物表达水平降低。GRb3可显著抑制DOX诱导的心肌炎症和氧化应激反应。G-Rb3对DOX诱导心肌毒性损伤具有保护作用主要通过激活PI3K/ AKT信号通路,而PI3K/AKT抑制剂Wortmanin可以逆转人参皂苷Rb3对心肌的保护作用。结论 人参皂苷Rb3可通过激活PI3K/AKT通路改善DOX诱导的心脏毒性。
关键词:  参皂苷Rb3  多柔比星  心肌毒性  炎症  氧化应激
DOI:
基金项目:湖北省自然科学基金项目(2017CFB211);湖北省卫生健康委科研项目(WJ2019Q011);黄石市2016年科技计划项目
The protective effects and potential mechanisms of ginsenoside Rb3 on doxorubicin induced cardiotoxicity
ZHANG Chenglian,XU Weipan,CAI Zhenxuan
(Department of Cardiology, Huangshi Central Hospital of Edong Healthcare Group Affiliated Hospital of Hubei Polutechnic Uiversity)
Abstract:
【Abstract】Objective To investigate the effect and mechanism of ginsenoside Rb3 in the development of Doxorubicin (DOX)induced cardiotoxicity. Methods SD rats were randomly divided into control group, DOX (25 mg/kg) group, DOX+ ginsenoside Rb3 (20 mg/Kg) and DOX+GRb3+ Wortmanin (1mg/Kg/d). The model of myocardial toxicity was established by intraperitoneal injection of DOX 6 times in 14 days. The protective effect of ginsenoside Rb3 on cardiotoxicity induced by DOX was observed. Myocardial pathological changes were observed by H&E staining in rats. The levels of myocardial injury markers, inflammatory factors, oxidative stress were detected by ELISA kit. The protein expression levels of pPI3K, PI3K, pAKT and AKT were detected by Western Blotting. Results DOXinduced cardiotoxicity resulted in increased myocardial damage and increased inflammation and oxidative stress. The GRb3 could improve the heart damage caused by DOX, mainly in the significant reduction of collagen accumulation and the decrease of myocardial injury marker levels. Simultaneous treatment with ginsenoside Rb3 significantly inhibited DOXinduced myocardial inflammation and oxidative stress. In the mechanism study, we found that ginsenoside Rb3 could activate PI3K/AKT signaling pathway in DOXinduced cardiotoxicity injury, and PI3K/AKT inhibitor Wortmanin could reverse the protective effect of ginsenoside Rb3 on myocardium. Conclusion Ginsenoside Rb3 can improve DOXinduced cardiotoxicity by activating the PI3K/AKT pathway.
Key words:  Ginsenoside Rb3  Doxorubicin  Cardiotoxicity  Inflammation  Oxidative stress

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