Tropical Journal of Pharmaceutical Research

Original Research Article | OPEN ACCESS

Physalin A alleviates inflammation and oxidative stress in mouse infantile pneumonia by inhibiting JAK/STAT3 and NF-κB; pathways

Zhenhua Ling, Jinhua Zhao

Department of Paediatrics, The First People's Hospital of Nantong City, Nantong, Jiangsu Province 226001, China;

For correspondence:- Jinhua Zhao Email: zhaojinhua_dr@163.com Tel:+8613773650608

Accepted: 28 January 2023 Published: 27 February 2023

Citation: Ling Z, Zhao J. Physalin A alleviates inflammation and oxidative stress in mouse infantile pneumonia by inhibiting JAK/STAT3 and NF-κB; pathways. Trop J Pharm Res 2023; 22(2):283-288 doi: 10.4314/tjpr.v22i2.9

© 2023 The authors.
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Abstract

Purpose: To investigate the effect of physalin A on infantile pneumonia in mice.

Methods: A mouse model of infantile pneumonia was established via intraperitoneal injection of lipopolysaccharide and verified using hematoxylin and eosin staining. Lipopolysaccharide-stimulated mice were then administered physalin A. The total protein content, number of cells, and levels of inflammatory-factor in bronchoalveolar lavage fluid (BALF) were determined. Inflammation and oxidative stress levels in lung tissues were determined by enzyme-linked immunosorbent assay (ELISA).

Results: Lipopolysaccharide injection induced shrinking of pulmonary alveoli in mice, but physalin A administration ameliorated the histopathologic damage in lung tissues and significantly reduced the total protein content and number of cells in the BALF of lipopolysaccharide-stimulated mice (p < 0.001). Moreover, physalin A also significantly down-regulated the levels of tumor necrosis factor-α, interleukin (IL)-6, IL-18, and IL-1β in BALF and lung tissues of lipopolysaccharide-treated mice (p < 0.001). Physalin A attenuated lipopolysaccharide-induced increases in malondialdehyde and myeloperoxidase as well as decreases in superoxide dismutase and glutathione in mouse lung tissues. Additionally, physalin A reduced the levels of p-JAK1, p-STAT3, and p-p65 in lung tissues of lipopolysaccharide-treated mice.

Conclusion: Physalin A exerts anti-inflammatory and anti-oxidant effect on lipopolysaccharide-induced lung injury in mice through the inactivation of JAK/STAT3 and NF-κB pathways. However, the effect of Physalin A on inflammation and oxidative stress in lipopolysaccharide-induced A549 cells will need to be investigated in further studies.

Keywords: Physalin A, Inflammation, Oxidative stress, Lipopolysaccharide, Lung injury, Infantile pneumonia