共 50 条
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
相关论文