Tropical Journal of Pharmaceutical Research

Original Research Article | OPEN ACCESS

Vitexin attenuates smoke inhalation-induced acute lung injury in rats by inhibiting oxidative stress via PKC β/p66Shc signaling pathway

Xuxin Chen^1,2, Huming Li¹, Hao Cheng¹, Meng Liu¹, Fan Wang¹, Jiguang Meng^1,2, Zhihai Han^1,2

¹Department of Pulmonary and Critical Care Medicine, The Sixth Medical Center of Chinese PLA General Hospital, Beijing 100037; ²School of Medicine, South China University of Technology, Guangzhou 510006, PR China.

For correspondence:- Zhihai Han Email: zhihaihandoctor@163.com

Accepted: 1 December 2022 Published: 29 December 2022

Citation: Chen X, Li H, Cheng H, Liu M, Wang F, Meng J, et al. Vitexin attenuates smoke inhalation-induced acute lung injury in rats by inhibiting oxidative stress via PKC β/p66Shc signaling pathway. Trop J Pharm Res 2022; 21(12):2507-2518 doi: 10.4314/tjpr.v21i12.2

© 2022 The authors.
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Abstract

Purpose: To investigate the protective effect of vitexin on smoke inhalation-induced acute lung injury (SI-ALI), and the underlying mechanism of action.

Methods: The ALI rat model was established by inhalation of smoke in a closed smoke chamber. Survival rate, arterial blood gas analysis, wet-to-dry weight ratio of lung tissues, bronchoalveolar lavage fluid protein concentration, lung tissue histology, and oxidative stress and inflammation level were evaluated. expressions of protein kinase C β (PKC β), p66Shc, and phosphorylated p66Shc were determined by western blot or quantitative reverse transcription-polymerase chain reaction.

Results: Compared with smoke inhalation group, vitexin alleviated the decline in arterial partial pressure of oxygen (p < 0.05), reduced lung tissue exudation and pathological lung tissue damage, inhibited the expression of PKC β/p66Shc signaling pathway proteins, downregulated the level of oxidative stress and inflammation, and ultimately improved the survival rate in SI-ALI rats (p < 0.05).

Conclusion: Vitexin attenuates SI-ALI in rats by alleviating oxidative stress via inhibition of PKC β/p66Shc signaling pathway. Thus, this compound is a potential agent for the treatment of SI-ALI.

Keywords: Vitexin, Smoke inhalation, Acute lung injury, Oxidative stress, p66Shc