Tetramethylpyrazine attenuates lipopolysaccharide-induced cardiomyocyte injury via improving mitochondrial function mediated by 14-3-3γ

被引:29
作者
Huang, Bowei [1 ]
You, Jiegeng [2 ]
Qiao, Yang [3 ]
Wu, Zelong [3 ]
Liu, Dan [3 ]
Yin, Dong [4 ]
He, Huan [3 ]
He, Ming [3 ]
机构
[1] Nanchang Univ, Jiangxi Med Sch, Nanchang 330006, Jiangxi, Peoples R China
[2] Nanchang Univ, Jiangxi Acad Med Sci, Nanchang 330006, Jiangxi, Peoples R China
[3] Nanchang Univ, Jiangxi Prov Key Lab Basic Pharmacol, Sch Pharmaceut Sci, Nanchang 330006, Jiangxi, Peoples R China
[4] Nanchang Univ, Affiliated Hosp 2, Jiangxi Prov Key Lab Mol Med, Nanchang 330006, Jiangxi, Peoples R China
基金
中国国家自然科学基金;
关键词
Tetramethylpyrazine; 14-3-3; gamma; Lipopolysaccharide; Cardioprotection; Mitochondrial function; NEONATAL-RAT CARDIOMYOCYTES; (ROS)-INDUCED ROS RELEASE; DYSFUNCTION ROLE; LIGUSTRAZINE; EXPRESSION; APOPTOSIS; PROTECTS; CELL; 14-3-3-PROTEINS; ANTIOXIDANT;
D O I
10.1016/j.ejphar.2018.05.019
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Lipopolysaccharide (LPS) is one of the many reasons that can cause myocardial injury. Our previous works have demonstrated that 14-3-3 gamma could protect myocardium against LPS-induced injury. Tetramethylpyrazine (TMP), an alkaloid found in Chinese herbs, exerts myocardial protection in many ways with multiple targets. We hypothesized that the cardioprotection of TMP against LPS-induced injury is attributed to upregulation of 14-3-3 gamma and improvement of mitochondrial function. To test the hypothesis, we investigated the effects of TMP on LPS-induced injury to cardiomyocytes by determining cell viability, LDH and caspase-3 activities, reactive oxygen species and MMP levels, mPTP openness, and apoptosis rate. The expression of 14-3-3 gamma and Bcl-2, and the phosphorylation of Bad (S112) were examined by Western blot. LPS-induced injury to cardiomyocytes was attenuated by TMP via upregulating expression of 14-3-3 gamma, and Bcl-2 on mitochondria, activating Bad (S112) phosphorylation, increasing cell viability and MMP levels, decreasing LDH and caspase-3 activity, reactive oxygen species generation, mPTP opening and apoptosis rate. However, the cardioprotection of TMP was attenuated by pAD/14-3-3 gamma-shRNA, an adenovirus that knocked down intracellular 14-3-3 gamma expression. In conclusion, the cardioprotection of TMP against LPS-induced injury was through up-regulating the expression of 14-3-3 gamma, promoting the translocation of Bcl-2 to mitochondria, and improving the function of mitochondria.
引用
收藏
页码:67 / 74
页数:8
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