Tropical Journal of Pharmaceutical Research

Original Research Article | OPEN ACCESS

Forsythiaside A inhibits hydrogen peroxide-induced inflammation, oxidative stress, and apoptosis of cardiomyocytes

Runqin Li , Dengfeng Ma, Zhihua Fu, Xiaoxuan Zheng, Wenxiu Li

Department of Cardiovascular Medicine, Taiyuan Central Hospital, Taiyuan City, Shanxi Province 030009, China;

For correspondence:- Runqin Li Email: rqli8046@163.com

Accepted: 28 September 2021 Published: 31 October 2021

Citation: Li R, Ma D, Fu Z, Zheng X, Li W. Forsythiaside A inhibits hydrogen peroxide-induced inflammation, oxidative stress, and apoptosis of cardiomyocytes. Trop J Pharm Res 2021; 20(10):2029-2034 doi: 10.4314/tjpr.v20i10.3

© 2021 The authors.
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Abstract

Purpose: To investigate the effect of forsythiaside A on heart failure.

Methods: An in vitro cell model of myocardial injury was established by incubating H9c2 primary cardiomyocytes with hydrogen peroxide (H₂O₂). Apoptosis was measured by flow cytometry. expression of inflammatory factors, including tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6), was determined by quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and enzyme-linked immunosorbent assay (ELISA). Oxidative stress was evaluated by measuring malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px) levels by ELISA.

Results: Incubation with H₂O₂ increased H9c2 cell apoptosis (p < 0.001). Treatment with forsythiaside A reduced Bax expression and enhanced Bcl-2 expression which suppressed apoptosis of H₂O₂-induced H9c2 cells. Forsythiaside A also attenuated the H₂O₂-induced increase in TNF-α and IL-6 expressions in H9c2 cells (p < 0.001). The H₂O₂-induced increase in MDA and decrease in SOD and GSH-Px in H9c2 cells were reversed by treatment with forsythiaside A. IκBα protein expression was downregulated, whereas p65 phosphorylation (p-p65), p-IκBα, nuclear factor erythropoietin-2-related factor 2 (Nrf2), and heme oxygenase 1 (HO-1) were upregulated in H₂O₂-induced H9c2 cells. Forsythiaside A increased IκBα, Nrf2, and HO-1 expression and decreased p-p65 and p-IκBα expression in H₂O₂-induced H9c2 cells.

Conclusion: Forsythiaside A exerts anti-inflammatory, anti-oxidant, and anti-apoptotic effects against H₂O₂-induced H9c2 cells through inactivation of NF-κB pathway and activation of Nrf2/HO-1 pathway. These results support the potential clinical application of forsythiaside A for the treatment of heart failure.

Keywords: Forsythiaside A, Inflammation, Oxidative stress, Apoptosis, Hydrogen peroxide, Cardiomyocytes