Abstract
Objectives: The present study aimed at investigating the therapeutic effect of Salidroside on skeletal muscle atrophy in a rat model of cigarette smoking-induced chronic obstructive pulmonary disease (COPD) and its potential mechanisms.Methods: Male Wistar rats were randomized, and treated intraperitoneally (IP) with vehicle (injectable water) or a low, medium or high dose of Salidroside, followed by exposure to cigarette smoking daily for 16 weeks. A healthy control received vehicle injection and air exposure. Their lung function, body weights and gastrocnemius (GN) weights, grip strength and cross-section area (CSA) of individual muscular fibers in the GN were measured. The levels of TNF-α, IL-6, malondialdehyde (MDA), superoxide dismutase (SOD), glutathione (GSH) in serum and GN tissues as well as myostatin and myogenin expression in GN tissues were measured.Results: In comparison with that in the healthy control, long-term cigarette smoking induced emphysema, significantly impaired lung function, reduced body and GN weights and CSA values in rats, accompanied by significantly increased levels of TNF-α, IL-6 and MDA, but decreased levels of SOD and GSH in serum and GN tissues. Furthermore, cigarette smoking significantly up-regulated myostatin expression, but down-regulated myogenin expression in GN tissues. Salidroside treatment decreased emphysema, significantly ameliorated lung function, increased antioxidant, but reduced MDA, IL-6 and TNF-α levels in serum and GN tissues of rats, accompanied by decreased myostain, but increased myogenin expression in GN tissues.Conclusion: Salidroside mitigates the long-term cigarette smoking-induced emphysema and skeletal muscle atrophy in rats by inhibiting oxidative stress and inflammatory responses and regulating muscle-specific transcription factor expression.
Highlights
Chronic obstructive pulmonary disease (COPD) is a commonly chronic inflammatory disease and it will be the third most dead disease worldwide in 2030 [1]
Further analyses indicated that the ratios of FEV0.2/forced vital capacity (FVC) and the values of peak expiratory flow (PEF) and mean alveolar number (MAN) were significantly reduced in the COPD group of rats (P
While the values of mean linear intercept (MLI) in the COPD group were significantly higher than the healthy control (P
Summary
Chronic obstructive pulmonary disease (COPD) is a commonly chronic inflammatory disease and it will be the third most dead disease worldwide in 2030 [1]. Long-term heavy smoking is a risk factor for the development of COPD. This, together with air pollution, increases the incidence of COPD in smoking population. Many harmful components in cigarettes can damage epithelial cells in the respiratory tract and vascular endothelial cells, and cause chronic inflammation, leading to respiratory and cardiovascular diseases [2]. Long-term heavy cigarette smoking and COPD can result in skeletal muscular. Atrophy, accelerating the pathogenic process of COPD [3]. The pathogenesis of COPD-related skeletal muscle atrophy is unclear and there is no effective therapy for intervention of COPD-related skeletal muscle atrophy.
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