Exploring the preventive effects of Jie Geng Tang on pulmonary fibrosis induced in vitro and in vivo: a network pharmacology approach.

Autor: Li B; School of Life Science, Huaibei Normal University, Dongshan Road 100, Huaibei, 235000, China., Jiang X; School of Life Science, Huaibei Normal University, Dongshan Road 100, Huaibei, 235000, China., Liu C; School of Life Science, Huaibei Normal University, Dongshan Road 100, Huaibei, 235000, China., Ma Y; School of Life Science, Huaibei Normal University, Dongshan Road 100, Huaibei, 235000, China., Zhao R; School of Life Science, Huaibei Normal University, Dongshan Road 100, Huaibei, 235000, China., Zhang H; School of Life Science, Huaibei Normal University, Dongshan Road 100, Huaibei, 235000, China. haijunzhang@163.com.
Jazyk: angličtina
Zdroj: Naunyn-Schmiedeberg's archives of pharmacology [Naunyn Schmiedebergs Arch Pharmacol] 2024 Dec; Vol. 397 (12), pp. 10005-10016. Date of Electronic Publication: 2024 Jul 03.
DOI: 10.1007/s00210-024-03262-w
Abstrakt: Pulmonary fibrosis is a debilitating lung disease marked by excessive fibrotic tissue accumulation, which significantly impairs respiratory function. Given the limitations of current therapies, there is an increasing interest in exploring traditional herbal formulations like Jie Geng Tang (JGT) for treatment. This study examines the potential of JGT and its bioactive component, quercetin, in reversing bleomycin (BLM)-induced pulmonary fibrosis in mice. We employed a BLM-induced MLE-12 cell damage model for in vitro studies and a bleomycin-induced fibrosis model in C57BL/6 mice for in vivo experiments. In vitro assessments showed that JGT significantly enhanced cell viability and reduced apoptosis in MLE-12 cells treated with BLM. These findings underscore JGT's potential for cytoprotection against fibrotic agents. In vivo, JGT was effective in modulating the expression of E-cadherin and vimentin, key markers of the epithelial-mesenchymal transition (EMT) pathway, indicating its role in mitigating EMT-associated fibrotic changes in lung tissue. Quercetin, identified through network pharmacology analysis as a potential key bioactive component of JGT, was highlighted for its role in the regulatory mechanisms underlying fibrosis progression, particularly through the modulation of the IL-17 pathway and Il6 expression. By targeting inflammatory pathways and key processes like EMT, JGT and quercetin offer a potent alternative to conventional therapies, meriting further clinical exploration to harness their full therapeutic potential in fibrotic diseases.
Competing Interests: Declarations. Ethics approval: This study was performed in line with the principles of the Declaration of Helsinki. Approval was granted by the Ethics Committee of The Liaoning Changsheng Biotechnology (CSE20201017). Consent to participate: Not applicable. Consent for publication: Not applicable. Competing interests: The authors declare no competing interests. Research involving animals: Male C57BL/6 mice, 5–7 weeks old, were sourced from Liaoning Changsheng Biotechnology (Approval No. SCXK(Liao)2020–00001). We divided the mice into five groups with seven animals each: control, BLM (5 mg/kg), two BLM + JGT-E groups treated with 50 mg/kg and 100 mg/kg, and BLM + PFD (100 mg/kg) group. After acclimating for 1 week, the JGT-E treatment was administered orally to the respective groups for 3 days. Mice designated for BLM treatment received a 5 mg/kg dose intratracheally, while controls were given saline. Both JGT-E and PFD treatments were continued daily, based on individual body weights. Three weeks later, the mice were euthanized for analysis.
(© 2024. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)
Databáze: MEDLINE
Externí odkaz: