Tropical Journal of Pharmaceutical Research

Original Research Article | OPEN ACCESS

Retinol exerts therapeutic effect on myocardial infarction through regulation of immune inflammatory cells and Cx43 expression

Hao Sun, Jiuchang Zhong, Xinchun Yang, Zongsheng Guo, Jiamei Liu, Boqia Xie, Yuan Zhang, Xin Wang, Linying Shi, Mulei Chen

Heart Centre, Beijing Chao-Yang Hospital, Capital Medical University, Beijing 100020, China;

For correspondence:- Mulei Chen Email: Mulechen20@yahoo.com Tel:+861065951480

Accepted: 19 April 2021 Published: 31 May 2021

Citation: Sun H, Zhong J, Yang X, Guo Z, Liu J, Xie B, et al. Retinol exerts therapeutic effect on myocardial infarction through regulation of immune inflammatory cells and Cx43 expression. Trop J Pharm Res 2021; 20(5):961-966 doi: 10.4314/tjpr.v20i5.11

© 2021 The authors.
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Abstract

Purpose: To investigate the effect of retinol on cardiac fibroblast proliferation in vitro and on fibrosis formation in mice in vivo.

Methods: Proliferative potential of fibroblasts was determined using cell counting kit-8 assay. Acute myocardial infarction (AMI) was induced in mice via ligation of the left side coronary artery. In myocardial tissues, concentration of TNF-α was determined using enzyme-linked immunosorbent assay (ELISA) assay.

Results: Exposure to retinol significantly suppressed cardiac fibroblast proliferation under ischemia, when compared to untreated fibroblasts (p < 0.05). However, exposure of cardiac fibroblasts to retinol did not produce toxicity at a dose of 10 µM under normal conditions. In contrast, exposure to normal levels of oxygen, glutamine and glucose significantly reversed the inhibitory potential of retinol against fibroblasts during ischemia (p < 0.05). Treatment of mice with retinol at a dose of 5 mg/kg reversed the AMI-mediated increase in hydroxyproline level in myocardial tissues. Retinol treatment of AMI mice caused significant elevation in the number of CD31+ capillaries in myocardial tissues. Increase in TNF-α by AMI in cardiac tissues of mice was reversed by treatment with retinol at a dose of 5 mg/kg. The retinol treatment also caused significant reversal of AMI-induced down-regulation of Cx43 protein (p < 0.05).

Conclusion: Retinol enhanced the proliferation of fibroblasts under ischemic conditions and prevented fibrosis in mice with AMI. Moreover, retinol targeted TNF-α production and upregulated Cx43 expression in myocardial tissues of mice with AMI. Thus, retinol may be useful for the management of myocardial infarction

Keywords: Myocardial infarction, Retinoic acid, Hydroxyproline, Myofibroblasts, Cell proliferation