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Protective Effect of Paeoniflorin on Hypoxia Reoxygenation Cardiomyocytes and its Mechanism Based on MAPK Signal Pathway

Protective Effect of Paeoniflorin on Hypoxia Reoxygenation Cardiomyocytes and its Mechanism Based on MAPK Signal Pathway

Shu-Zhi Qin, Wen-Pei Ling, Mei-Fang Yin, Chun-Yu Luo and Cheng-Guo Zhao*

College of Pharmacy and Food Science, Zhuhai College of Science and Technology, Zhuhai 519041, China

 
* Corresponding author: zcg@zcst.edu.cn

ABSTRACT

Mitogen-activated protein kinases (MAPK) is an important signal pathway involved in cardiomyocyte injury. To investigate the protective effect of paeoniflorin (PF) on hypoxia reoxygenation (H/R) injury and its effect on MAPK signal pathway to reveal the mechanism of PF against myocardial ischemia-reperfusion injury, in this study, the H/R model of H9C2 cells was established by hypoxia for 3 h and reoxygenation for 3 h. H9C2 cells were divided into 4 groups, the control, PF + control group, H/R group and H/R + PF group. The activities of aspartate aminotransferase (AST) and lactate dehydrogenase (LDH) were measured by colorimetry; Apoptosis rate and reactive oxygen species (ROS) content were measured by flow cytometry; the expression of Bcl-2, Caspase-3, p38 MAPK, ERK1/2 and JNK proteins were determined by WB technique. The results showed that, compared with control group, LDH, AST content, ROS level, apoptosis rate, Caspase-3, p38 MAPK, ERK1/2, JNK protein expression in H/R group were significantly increased, while cell survival rate and Bcl-2 protein expression were significantly decreased (P <0.05). Moreover, compared with H/R group, H/R+PF group could reduce the levels of AST, LDH, ROS (P <0.05), reduce the apoptosis rate and the expression of p38 MAPK, ERK1/2, JNK proteins (P <0.05), and increase the cell survival rate and the expression of Bcl-2 protein (P <0.05). In conclusion, PF can protect H9C2 cells from H/R injury, which may be related to regulating the expression of MAPK pathway.

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Pakistan Journal of Zoology

February

Pakistan J. Zool., Vol. 56, Iss. 1, pp. 01-501

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