Tropical Journal of Pharmaceutical Research

Original Research Article | OPEN ACCESS

Citrate pre-conditioning inhibits apoptosis and protects rat myocardium from ischemia-reperfusion injury by activating PI3K/Akt signaling pathway

Zhiyun Zhu¹, Fugen Nie², Bo Qiu³, Diqin Wan⁴, Wenfeng Duan⁵

¹Department of Cardiology, Jiangxi Provincial People's Hospital, The First Affiliated Hospital of Nanchang Medical College, Nanchang 330006, China; ²Department of Cardiology, The Third Hospital of Nanchang, Nanchang 330008, China; ³Department of Cardiology, Zhangshu People's Hospital, Zhangshu 331299, China; ⁴Department of Emergency, Anyi County People's Hospital, Anyi 330500, China; ⁵Department of Imaging, The First Affiliated Hospital of Nan Chang University, Nanchang 330006, Jiangxi Province, China.

For correspondence:- Wenfeng Duan Email: zhuzhiyun2022@163.com

Accepted: 23 December 2022 Published: 31 January 2023

Citation: Zhu Z, Nie F, Qiu B, Wan D, Duan W. Citrate pre-conditioning inhibits apoptosis and protects rat myocardium from ischemia-reperfusion injury by activating PI3K/Akt signaling pathway. Trop J Pharm Res 2023; 22(1):215-221 doi: 10.4314/tjpr.v22i1.29

© 2023 The authors.
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Abstract

Purpose: To study the influence of citric acid pre-exposure on apoptosis and heart tissue ischemia-reperfusion lesion, and the involvement of PI3K/Akt signal route in this process.

Methods: Eighty-four male Sprague-Dawley (SD) rats were randomly divided into a sham group, model group, pretreatment group, and inhibitor group, with 21 rats in each group. Changes in myocardial infarction area were determined using TCC staining, while TUNEL assay was performed to assess apoptosis of cardiomyocytes in the rats. expression levels of p-Akt, ppi3k, Bcl-2, Bax, and caspase-3 were assayed by Western blotting.

Results: The levels of Bax and caspase-3 were higher in model rats than in sham group, while concentrations of Bcl-2, p-Akt, and p-pi3k were significantly reduced. In pre-treated and inhibitor-exposed rats, caspase-3 and Bax levels were significantly down-regulated, relative to corresponding levels in model rats, but Bcl-2, p-pi3k, and p-Akt were significantly up-regulated (p < 0.05). In inhibitor-exposed rats, Bax and caspase-3 were higher than levels in pretreatment rats, but p-pi3k, Bcl-2, and p-Akt concentrations were significantly decreased (p < 0.05).

Conclusion: Citric acid pretreatment in rats activates PI3K/Akt signal pathway, inhibits cardiomyocyte apoptosis, protects the myocardium from ischemia-reperfusion injury, and improves cardiac function. The potential of citric acid pretreatment for its protective effect against myocardial injury due to ischemia-reperfusion should be further investigated.

Keywords: Citric acid, Pretreatment, PI3K/Akt signal pathway, Apoptosis, Myocardial ischemia-reperfusion