文献类型：期刊文献

英文题名：Codonopsis Radix Inhibits the Inflammatory Response and Oxidative Stress in Chronic Obstructive Pulmonary Disease Mice through Regulation of the Nrf2/NF-κB Signaling Pathway

作者：Chen, Zhengjun[1];Shi, Qi[1];Liu, Xuxia[1];Lu, Guodi[1];Yang, Jie[2];Luo, Wenrong[3];Yang, Fude[1]

第一作者：陈正君

通信作者：Yang, FD[1]

机构：[1]Gansu Univ Chinese Med, Pharm Coll, Lanzhou, Peoples R China;[2]Beijing Univ Chinese Med, Beijing, Peoples R China;[3]Gansu Prov Hosp Tradit Chinese Med, Lanzhou, Peoples R China

第一机构：甘肃中医药大学

通信机构：[1]corresponding author), Gansu Univ Chinese Med, Pharm Coll, Lanzhou, Peoples R China.|[10735]甘肃中医药大学;

年份：2024

外文期刊名：PHARMACOLOGY

收录：;WOS:【SCI-EXPANDED(收录号:WOS:001252735700001)】；

基金：This research was supported by the Science and Technology Project of Gansu Province (No. 21JR1RA271), the Key Research and Development Project of the Ministry of Science and Technology (No.2018YFC1706305), the Industrial Support Program of Colleges and Universities in Gansu Province (No.2021CYZC-40),and the "Innovation Star"Program for graduate students of Gansu Provincial Education Department (No.2023CXZX-740), Natural Fund Project of Science and Technology Department of Gansu Province (No.22JR5RA592), Young Doctor Fund Project of Gansu Provincial Department of Education (No.2022QB-099).

语种：英文

外文关键词：Codonopsis Radix; Cigarette smoke extract; Inflammation; Chronic obstructive pulmonary disease; Nuclear factor-related factor 2/nuclear transcription factor-kappa B signaling pathway

摘要：Introduction: Chronic obstructive pulmonary disease (COPD) is a nonspecific chronic inflammatory lung disease with no known cure. Codonopsis Radix (CR) has been shown to exhibit anti-inflammatory and antioxidant effects. Therefore, this study aimed to investigate the potential anti-inflammatory effects of different CR varieties on COPD mice. Methods: Sixty male-specified pathogen-free grade C57BL/6J mice were randomly divided into 6 groups, 10 mice in each group. The COPD mice model was induced by cigarette smoke extract combined with lipopolysaccharide, and the mice in each group were given corresponding drugs. Lung function was assessed in all mice. Lung tissues were stained with hematoxylin-eosin, Masson, and periodic acid-Schiff stains, and serum levels of interleukin (IL)-8 and tumor necrosis factor (TNF)-alpha were detected using an ELISA. Further, serum and lung tissue levels of malondialdehyde (MDA) and superoxide dismutase (SOD) were detected by colorimetric assay. Network pharmacology and molecular docking were used to predict signaling pathways, which were validated by Western blot analysis. Results: Compared with the COPD group, the mice in each dosing group of CR exhibited significant reductions in serum IL-8 and TNF-alpha levels, serum and lung tissue MDA levels, and pathological lung tissue damage, alongside elevations in lung function and SOD levels (p < 0.01). Western blot analysis also indicated significant downregulation of p-p65/p65 and p-I kappa B-alpha/I kappa B-alpha protein expression, alongside significant upregulation of Nrf2 protein expression in the lung tissues of mice treated with CR (p < 0.01). Conclusion: In summary, CR effectively enhances lung function, minimizes lung tissue damage, and inhibits inflammation and oxidative stress in mice with COPD. Additionally, these findings suggest that inhibition of the Nrf2/NF-kappa B axis may be a key mechanism of action of CR in the alleviation of COPD. (c) 2024 S. Karger AG, Basel