Tropical Journal of Pharmaceutical Research

Original Research Article | OPEN ACCESS

Salvianolic acid A regulates Nrf2 and NF-κB pathways to alleviate lipopolysaccharide-induced pneumonia cell damage

Hai Lin¹, Jinrong Yi²

¹Department of Respiratory and Critical Care Medicine, First Affiliated Hospital of Gannan Medical University, Jiangxi Province 341000, China; ²Department of Anesthesiology, Ganzhou Women and Childrenâ€™s Health Care Hospital, Ganzhou City, Jiangxi Province 341000, China.

For correspondence:- Jinrong Yi Email: jryi5467@163.com Tel:+8615607979653

Accepted: 23 May 2023 Published: 30 June 2023

Citation: Lin H, Yi J. Salvianolic acid A regulates Nrf2 and NF-κB pathways to alleviate lipopolysaccharide-induced pneumonia cell damage. Trop J Pharm Res 2023; 22(6):1167-1171 doi: 10.4314/tjpr.v22i6.4

© 2023 The authors.
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Abstract

Purpose: To examine the regulatory roles of salvianolic acid A (SA-A) in lipopolysaccharide-induced pneumonia cell damage.

Methods: Cell proliferation in lung epithelial cells BEAS-2B was determined using CCK-8 assay while cell apoptosis was assessed by flow cytometry. The levels of TNF-α, IL-1β and IL-6 were determined using enzyme-linked immunosorbent assay (ELISA). Protein expressions were evaluated using western blot, while the levels of superoxide dismutase (SOD), myeloperoxidase (MPO), and malondialdehyde (MDA) were assessed using their corresponding ELISA kits.

Results: Cell apoptosis was enhanced after LPS induction (p < 0.001), but this change was offset after SA-A treatment (p < 0.05). Inflammation was increased after LPS stimulation (p < 0.001), but this change was offset following SA-A treatment (p < 0.05). Oxidative stress was heightened after LPS induction (p < 0.05), but reversed following SA-A treatment (p < 0.05). Finally, LPS stimulation enhanced endoplasmic reticulum stress and mitochondrial dysfunction (p < 0.001), which was significantly reversed by SA-A treatment (p < 0.05).

Conclusion: SA-A regulates Nrf2 and NF-κB pathways, inhibits oxidative stress, inflammation-stimulated ER stress, and mitochondrial dysfunction. It also alleviates LPS-induced pneumonia cell damage, thus indicating its potentials for development as a therapeutic agent for the treatment of pneumonia.

Keywords: Salvianolic acid A, Inflammation, Oxidative stress, Lipopolysaccharide, Pneumonia