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Original Articles

Compound glycyrrhiza oral solution alleviates oxidative stress and inflammation by regulating SRC/MAPK pathway in chronic obstructive pulmonary disease

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Pages 1032-1043 | Received 24 Feb 2022, Accepted 09 Jul 2022, Published online: 11 Aug 2022
 

Abstract

Objectives

Patients with chronic obstructive pulmonary disease (COPD) suffer from persistent cough and breathlessness, which can be ameliorated by the Chinese herbal medicine glycyrrhiza. Furthermore, the SRC/MAPK pathway is activated in the process of oxidative stress and inflammation, which afflict COPD progression. Thus, this research aimed at dissecting the mechanism of compound glycyrrhiza oral solution (CGOS) relieving oxidative stress and inflammation in COPD via the SRC/MAPK pathway.

Methods

After a COPD rat model was established using lipopolysaccharide and cigarette smoke, rats underwent intragastric administration with CGOS and intratracheal injection with LV-NC and LV-SRC lentivirus into lungs. Then, pulmonary function-related indexes were evaluated, followed by analyses of arterial blood and inflammatory cell number in prepared bronchoalveolar lavage fluids. Meanwhile, the contents of oxidative stress-related indicators (malondialdehyde, 3NT, 8-Isoprostane, glutathione, NO, and SOD) in pulmonary tissues were measured, along with RT-qPCR and ELISA detection of the expression of inflammatory factors (TNF-α, IL-1β, IL-4, and IL-10). Moreover, western blot assay was utilized to assess p-SRC/SRC and p-p38/p38 ratios in pulmonary tissues.

Results

CGOS treatment enhanced PaO2 and reduced PaCO2 in COPD rats, accompanied by declines in the number of total cells, neutrophils, and macrophages. CGOS improved pulmonary function, decreased malondialdehyde, 3NT, 8-Isoprostane, TNF-α, and IL-1β levels, and increased GSH, NO, IL-4, and IL-10 levels and SOD activity. Mechanistically, CGOS suppressed the SRC/MAPK pathway, and SRC overexpression reversed the alleviating function of CGOS in COPD rats.

Conclusions

In conclusion, CGOS might alleviate oxidative stress and inflammation in COPD rats by inhibiting the SRC/MAPK pathway.

Acknowledgement

The authors thank the section chief YaBin Ma for his valuable comments on the article, Dongfang Hospital and Tongji University for providing the experimental site/reagent supplies free of charge, and the hospital leadership for their support.

Disclosure statement

No potential conflict of interest was reported by the author(s).

Additional information

Funding

The author(s) reported there is no funding associated with the work featured in this article.

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