Soyasaponin I alleviates inflammation and oxidative stress in chronic obstructive pulmonary disease through inhibiting the MAPK signaling pathway.

IF 2.2 4区 农林科学 Q1 VETERINARY SCIENCES
Ruoqi Zhang, Jiabo Yuan, Congyao Wang, Ruiqi Zhao, Fengli Gao, Zhuying Li
{"title":"Soyasaponin I alleviates inflammation and oxidative stress in chronic obstructive pulmonary disease through inhibiting the MAPK signaling pathway.","authors":"Ruoqi Zhang, Jiabo Yuan, Congyao Wang, Ruiqi Zhao, Fengli Gao, Zhuying Li","doi":"10.1538/expanim.25-0007","DOIUrl":null,"url":null,"abstract":"<p><p>Chronic obstructive pulmonary disease (COPD) is a prevalent lung disease that mainly induced by cigarette smoking (CS). Soyasaponin I is an amphiphilic oleanane triterpenoid glycoside extracted form Astragali Radix. In order to investigate treatment strategies of COPD, this study focused on the effect of soyasaponin I on the lung tissue of COPD model. The mouse model of COPD was induced by CS exposure for 12 weeks, and was administrated with different doses of soyasaponin I. Subsequently, the morphology and histopathology of lung tissue, the proportion of inflammatory cell, the levels of inflammatory cytokines, and indicators of oxidative stress were assessed and analyzed. The signaling pathway potentially regulated by soyasaponin I in the pathogenesis of COPD were predicted by network pharmacology analysis and validated by western blot. Our results demonstrated that soyasaponin I mitigated the lung injury and bronchial lesions induced by COPD through reducing the lung coefficient, wall area of the bronchioles and Periodic Acid Schiff (PAS)-positive cells in the lung tissue. The CS-induced inflammation and oxidative stress was alleviated by soyasaponin I through reversing the levels of inflammatory cytokines and oxidative stress indicators. In addition, the phosphorylation of p38, JNK and ERK1/2 was activated in COPD model, and was reverted by soyasaponin I in the lung tissue. Collectively, the present study confirmed that soyasaponin I is an effective compound that attenuates the lung injury through inhibiting inflammatory response and oxidative stress via the MAPK signaling pathway.</p>","PeriodicalId":12102,"journal":{"name":"Experimental Animals","volume":" ","pages":""},"PeriodicalIF":2.2000,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Experimental Animals","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1538/expanim.25-0007","RegionNum":4,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"VETERINARY SCIENCES","Score":null,"Total":0}
引用次数: 0

Abstract

Chronic obstructive pulmonary disease (COPD) is a prevalent lung disease that mainly induced by cigarette smoking (CS). Soyasaponin I is an amphiphilic oleanane triterpenoid glycoside extracted form Astragali Radix. In order to investigate treatment strategies of COPD, this study focused on the effect of soyasaponin I on the lung tissue of COPD model. The mouse model of COPD was induced by CS exposure for 12 weeks, and was administrated with different doses of soyasaponin I. Subsequently, the morphology and histopathology of lung tissue, the proportion of inflammatory cell, the levels of inflammatory cytokines, and indicators of oxidative stress were assessed and analyzed. The signaling pathway potentially regulated by soyasaponin I in the pathogenesis of COPD were predicted by network pharmacology analysis and validated by western blot. Our results demonstrated that soyasaponin I mitigated the lung injury and bronchial lesions induced by COPD through reducing the lung coefficient, wall area of the bronchioles and Periodic Acid Schiff (PAS)-positive cells in the lung tissue. The CS-induced inflammation and oxidative stress was alleviated by soyasaponin I through reversing the levels of inflammatory cytokines and oxidative stress indicators. In addition, the phosphorylation of p38, JNK and ERK1/2 was activated in COPD model, and was reverted by soyasaponin I in the lung tissue. Collectively, the present study confirmed that soyasaponin I is an effective compound that attenuates the lung injury through inhibiting inflammatory response and oxidative stress via the MAPK signaling pathway.

大豆皂苷I通过抑制MAPK信号通路减轻慢性阻塞性肺疾病的炎症和氧化应激。
慢性阻塞性肺疾病(COPD)是一种主要由吸烟引起的常见肺部疾病。大豆皂苷I是从黄芪中提取的两亲性齐墩烷三萜苷。为了探讨慢性阻塞性肺病的治疗策略,本研究重点研究大豆皂苷I对慢性阻塞性肺病模型肺组织的影响。建立慢性阻塞性肺病小鼠模型,CS暴露12周后,给予不同剂量的大豆皂苷i,观察肺组织形态学和组织病理学变化、炎症细胞比例、炎症细胞因子水平及氧化应激指标。通过网络药理学分析预测大豆皂苷I在COPD发病过程中可能调控的信号通路,并通过western blot验证。我们的研究结果表明,大豆皂苷I通过降低肺系数、细支气管壁面积和肺组织中周期性酸席夫(PAS)阳性细胞来减轻慢性阻塞性肺疾病引起的肺损伤和支气管病变。大豆皂苷I通过逆转炎症因子和氧化应激指标水平,减轻cs诱导的炎症和氧化应激。此外,p38、JNK和ERK1/2的磷酸化在COPD模型中被激活,并在肺组织中被大豆皂苷I逆转。总之,本研究证实大豆皂苷I是一种有效的化合物,通过MAPK信号通路抑制炎症反应和氧化应激,从而减轻肺损伤。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
Experimental Animals
Experimental Animals 生物-动物学
CiteScore
2.80
自引率
4.20%
发文量
2
审稿时长
3 months
期刊介绍: The aim of this international journal is to accelerate progress in laboratory animal experimentation and disseminate relevant information in related areas through publication of peer reviewed Original papers and Review articles. The journal covers basic to applied biomedical research centering around use of experimental animals and also covers topics related to experimental animals such as technology, management, and animal welfare.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信