4.7 Article

Network Pharmacology and Experimental Assessment to Explore the Pharmacological Mechanism of Qimai Feiluoping Decoction Against Pulmonary Fibrosis

期刊

FRONTIERS IN PHARMACOLOGY
卷 12, 期 -, 页码 -

出版社

FRONTIERS MEDIA SA
DOI: 10.3389/fphar.2021.770197

关键词

COVID-19; pulmonary fibrosis; QM formula; network pharmacology; epithelial-mesenchymal transition; extracellular matrix accumulation; TGF-beta 1/Smad3 pathwey

资金

  1. National Natural Science Foundation of China
  2. Key Research and Development Program of Jilin Province
  3. Special Project for Emergency of the Ministry of Science and Technology

向作者/读者索取更多资源

Research has shown that Qimai Feiluoping decoction (QM) can improve PF symptoms in COVID-19 convalescent patients by regulating epithelial-mesenchymal transition, extracellular matrix degradation, and the TGF-beta signaling pathway. QM contains multiple active components and exerts its anti-PF effects by inhibiting the TGF-beta/Smad3 pathway.
Pulmonary fibrosis (PF) is one of the pathologic changes in COVID-19 patients in convalescence, and it is also a potential long-term sequela in severe COVID-19 patients. Qimai Feiluoping decoction (QM) is a traditional Chinese medicine formula recommended in the Chinese national medical program for COVID-19 convalescent patients, and PF is one of its indications. Through clinical observation, QM was found to improve the clinical symptoms and pulmonary function and reduce the degree of PF of COVID-19 convalescent patients. To further explore the pharmacological mechanisms and possible active components of QM in anti-PF effect, UHPLC/Q-TOF-MS was used to analyze the composition of the QM extract and the active components that can be absorbed into the blood, leading to the identification of 56 chemical compounds and 10 active components. Then, network pharmacology was used to predict the potential mechanisms and targets of QM; it predicted that QM exerts its anti-PF effects via the regulation of the epithelial-mesenchymal transition (EMT), extracellular matrix (ECM) degradation, and TGF-beta signaling pathway. Finally, TGF-beta 1-induced A549 cells were used to verify and explore the pharmacological effects of QM and found that QM could inhibit the proliferation of TGF-beta 1-induced A549 cells, attenuate EMT, and promote ECM degradation by inhibiting the TGF-beta/Smad3 pathway.

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