Asiatic Acid Protects against Doxorubicin-Induced Cardiotoxicity in Mice

被引:19
|
作者
Hu, Xiaoping [1 ]
Li, Baijun [2 ]
Li, Luocheng [1 ]
Li, Bowen [1 ]
Luo, Jinlong [2 ]
Shen, Bin [2 ]
机构
[1] Wuhan Univ, Renmin Hosp, Dept Cardiovasc Surg, Wuhan 430060, Hubei, Peoples R China
[2] Peoples Hosp Guangxi Zhuang Autonomous Reg, Dept Thorac Cardiovasc Surg, Nanning, Guangxi Zhuang, Peoples R China
基金
中国国家自然科学基金;
关键词
ANTHRACYCLINE CARDIOTOXICITY; CARDIAC DYSFUNCTION; OXIDATIVE STRESS; CELL-DEATH; ACTIVATION; INJURY; ANTIOXIDANTS; INFLAMMATION; ADRIAMYCIN; TOXICITY;
D O I
10.1155/2020/5347204
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
The use of doxorubicin (DOX) can result in depression of cardiac function and refractory cardiomyopathy. Currently, there are no effective approaches to prevent DOX-related cardiac complications. Asiatic acid (AA) has been reported to provide cardioprotection against several cardiovascular diseases. However, whether AA could attenuate DOX-related cardiac injury remains unclear. DOX (15 mg/kg) was injected intraperitoneally into the mice to mimic acute cardiac injury, and the mice were given AA (10 mg/kg or 30 mg/kg) for 2 weeks for protection. The data in our study found that AA-treated mice exhibited attenuated cardiac injury and improved cardiac function in response to DOX injection. AA also suppressed myocardial oxidative damage and apoptosis without affecting cardiac inflammation in DOX-treated mice. AA also provided protection in DOX-challenged cardiomyocytes, improved cell viability, and suppressed intracellular reactive oxygen species (ROS) in vitro. Detection of signaling pathways showed that AA activated protein kinase B (AKT) signaling pathway in vivo and in vitro. Furthermore, we found that AA lost its protective effects in the heart with AKT inactivation. In conclusion, our results found that AA could attenuate DOX-induced myocardial oxidative stress and apoptosis via activation of the AKT signaling pathway.
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页数:12
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