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甘草皂苷G2通过靶向肿瘤坏死因子-α信号通路并抑制上皮-间质转化来改善博来霉素诱导的肺纤维化。

Licoricesaponin G2 ameliorates bleomycin-induced pulmonary fibrosis via targeting TNF-α signaling pathway and inhibiting the epithelial-mesenchymal transition.

作者信息

Ma Jing, Ding Lu, Zang Xiaoyu, Wei Ruonan, Yang Yingying, Zhang Wei, Su Hang, Li Xueyan, Li Min, Sun Jun, Zhang Zepeng, Wang Zeyu, Zhao Daqing, Li Xiangyan, Zhao Linhua, Tong Xiaolin

机构信息

College of Traditional Chinese Medicine, Changchun University of Chinese Medicine, Changchun, China.

Key Laboratory of Active Substances and Biological Mechanisms of Ginseng Efficacy, Jilin Provincial Key Laboratory of Bio-Macromolecules of Chinese Medicine, Ministry of Education, Northeast Asia Research Institute of Traditional Chinese Medicine, Changchun University of Chinese Medicine, Changchun, China.

出版信息

Front Pharmacol. 2024 Sep 5;15:1437231. doi: 10.3389/fphar.2024.1437231. eCollection 2024.

DOI:10.3389/fphar.2024.1437231
PMID:39301567
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11412005/
Abstract

BACKGROUND

Pulmonary fibrosis (PF) emerges as a significant pulmonary sequelae in the convalescent phase of coronavirus disease 2019 (COVID-19), with current strategies neither specifically preventive nor therapeutic. Licoricesaponin G2 (LG2) displays a spectrum of natural activities, including antibacterial, anti-inflammatory, and antioxidant properties, and has been effectively used in treating various respiratory conditions. However, the potential protective effects of LG2 against PF remain underexplored.

METHODS

Network analysis and molecular docking were conducted in combination to identify the core targets and pathways through which LG2 acts against PF. In the model of bleomycin (BLM)-induced C57 mice and transforming growth factor-β1 (TGF-β1)-induced A549 and MRC5 cells, techniques such as western blot (WB), quantitative Real-Time PCR (qPCR), Immunohistochemistry (IHC), Immunofluorescence (IF), and Transwell migration assays were utilized to analyze the expression of Epithelial-mesenchymal transition (EMT) and inflammation proteins. Based on the analysis above, we identified targets and potential mechanisms underlying LG2's effects against PF.

RESULTS

Network analysis has suggested that the mechanism by which LG2 combats PF may involve the TNF-α pathway. Molecular docking studies have demonstrated a high binding affinity of LG2 to TNF-α and MMP9. Observations from the study indicated that LG2 may mitigate PF by modulating EMT and extracellular matrix (ECM) remodeling. It is proposed that the therapeutic effect is likely arises from the inhibition of inflammatory expression through regulation of the TNF-α pathway.

CONCLUSION

LG2 mitigates PF by suppressing TNF-α signaling pathway activation, modulating EMT, and remodeling the ECM. These results provide compelling evidence supporting the use of LG2 as a potential natural therapeutic agent for PF in clinical trials.

摘要

背景

肺纤维化（PF）是2019冠状病毒病（COVID-19）康复期出现的一种严重肺部后遗症，目前的策略既无特异性预防作用也无治疗作用。甘草皂苷G2（LG2）具有一系列天然活性，包括抗菌、抗炎和抗氧化特性，并已有效用于治疗各种呼吸道疾病。然而，LG2对PF的潜在保护作用仍未得到充分探索。

方法

联合进行网络分析和分子对接，以确定LG2抗PF作用的核心靶点和途径。在博来霉素（BLM）诱导的C57小鼠模型以及转化生长因子-β1（TGF-β1）诱导的A549和MRC5细胞中，利用蛋白质免疫印迹法（WB）、定量实时聚合酶链反应（qPCR）、免疫组织化学（IHC）、免疫荧光（IF）和Transwell迁移试验等技术分析上皮-间质转化（EMT）和炎症蛋白的表达。基于上述分析，我们确定了LG2抗PF作用的靶点和潜在机制。

结果

网络分析表明，LG2对抗PF的机制可能涉及肿瘤坏死因子-α（TNF-α）途径。分子对接研究表明LG2与TNF-α和基质金属蛋白酶9（MMP9）具有高结合亲和力。研究观察结果表明，LG2可能通过调节EMT和细胞外基质（ECM）重塑来减轻PF。推测其治疗作用可能源于通过调节TNF-α途径抑制炎症表达。

结论

LG2通过抑制TNF-α信号通路激活、调节EMT和重塑ECM来减轻PF。这些结果提供了有力证据，支持在临床试验中将LG2用作PF的潜在天然治疗药物。

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