Integration of metabolomics and network pharmacology to reveal the protective mechanism underlying Qibai Pingfei capsule on chronic obstructive pulmonary disease

Frontiers in Pharmacology

Pharmacology

Yating Gao¹  Zegeng Li¹  Jiabing Tong²  Mengxiang Liu³  Changan Liu³  Jinghui Xie³  Jie Zhu⁴  Fan Wu⁵ 

[1] Center for Xin’an Medicine and Modernization of Traditional Chinese Medicine, Institute of Health and Medicine, Anhui University of Chinese Medicine, Hefei, China;The First Affiliated Hospital of Anhui University of Traditional Chinese Medicine, Hefei, Anhui, China;Center for Xin’an Medicine and Modernization of Traditional Chinese Medicine, Institute of Health and Medicine, Anhui University of Chinese Medicine, Hefei, China;The First Affiliated Hospital of Anhui University of Traditional Chinese Medicine, Hefei, Anhui, China;College of Traditional Chinese Medicine, Anhui University of Chinese Medicine, Hefei, Anhui, China;College of Integrated Chinese and Western Medicine, Anhui University of Chinese Medicine, Hefei, Anhui, China;College of Integrated Chinese and Western Medicine, Anhui University of Chinese Medicine, Hefei, Anhui, China;Center for Xin’an Medicine and Modernization of Traditional Chinese Medicine, Institute of Health and Medicine, Anhui University of Chinese Medicine, Hefei, China;Institutes of Integrative Medicine, Fudan University, Shanghai, China;College of Traditional Chinese Medicine, Anhui University of Chinese Medicine, Hefei, Anhui, China;

关键词: COPD;    Qibai Pingfei capsule;    metabolomics;    network pharmacology;    ferroptosis;    glutathione metabolism;   

DOI  :  10.3389/fphar.2023.1258138

 received in 2023-07-13, accepted in 2023-10-09,  发布年份 2023

来源: Frontiers

【 摘 要 】

In this study, we have employed metabolomics technology in combination with network pharmacology to ascertain the key metabolites and hub genes. The objective was to explore the pathway of Qibai Pingfei Capsule (QBPF) in treating COPD through metabolomics. We identified 96 differential metabolites in the lung tissues of rats belonging to control and model groups, out of which 47 were observed to be critical (VIP >2, p < 0.05). Furthermore, 16 important differential metabolites were reversed after QBPF treatment. Using network pharmacology, we identified 176 core targets of 81 drug-active ingredients. Our comprehensive analysis of network pharmacology and metabolomics enabled us to identify a core target, prostaglandin-endoperoxide synthase 2 (PTGS2), and a core metabolic pathway for glutathione metabolism. Finally, the result of molecular docking showed that PTGS2 had strong binding activity to 18 compounds including Fumarine and Kaempferol, etc.. PTGS2 is a marker of ferroptosis, so we wanted to explore whether QBPF could inhibit ferroptosis in COPD. The results showed that ferroptosis was involved in the pathogenesis of COPD, and QBPF could inhibit the occurrence of ferroptosis. In conclusion, the mechanism of QBPF for treating COPD may be related to PTGS2 expression, glutathione metabolism and ferroptosis.

【 授权许可】

Unknown   
Copyright © 2023 Xie, Liu, Gao, Liu, Wu, Tong, Li and Zhu.