Salidroside Ameliorates Lung Injury Induced by PM _2.5by Regulating SIRT1-PGC-1α in Mice.

Biomedical and environmental sciences : BES Pub Date : 2024-04-20 DOI:10.3967/bes2024.041

Xiao Hong Li, Yu Mei Liu, Hui Shan, Jin Feng Tan, Jian Zhou, Yuan Jin Song, Si Qi Li, Chen Liu, Dong Qun Xu, Li Yu, Wan Wei Li

{"title":"Salidroside Ameliorates Lung Injury Induced by PM 2.5by Regulating SIRT1-PGC-1α in Mice.","authors":"Xiao Hong Li, Yu Mei Liu, Hui Shan, Jin Feng Tan, Jian Zhou, Yuan Jin Song, Si Qi Li, Chen Liu, Dong Qun Xu, Li Yu, Wan Wei Li","doi":"10.3967/bes2024.041","DOIUrl":null,"url":null,"abstract":"Objective: This study aimed to clarify the intervention effect of salidroside (SAL) on lung injury caused by PM 2.5 in mice and illuminate the function of SIRT1-PGC-1ɑ axis.Methods: Specific pathogen-free (SPF) grade male C57BL/6 mice were randomly assigned to the following groups: control group, SAL group, PM 2.5 group, SAL+PM 2.5 group. On the first day, SAL was given by gavage, and on the second day, PM 2.5 suspension was given by intratracheal instillation. The whole experiment consist of a total of 10 cycles, lasting 20 days. At the end of treatment, blood samples and lung tissues were collected and analyzed. Observation of pathological changes in lung tissue using inverted microscopy and transmission electron microscopy. The expression of inflammatory, antioxidants, apoptosis, and SIRT1-PGC-1ɑ proteins were detected by Western blotting.Results: Exposure to PM 2.5 leads to obvious morphological and pathologica changes in the lung of mice. PM 2.5 caused a decline in levels of antioxidant-related enzymes and protein expressions of HO-1, Nrf2, SOD2, SIRT1 and PGC-1ɑ, and an increase in the protein expressions of IL-6, IL-1β, Bax, caspase-9 and cleaved caspase-3. However, SAL reversed the aforementioned changes caused by PM 2.5 by activating the SIRT1-PGC-1α pathway.Conclusion: SAL can activate SIRT1-PGC-1ɑ to ameliorate PM 2.5-induced lung injury.","PeriodicalId":93903,"journal":{"name":"Biomedical and environmental sciences : BES","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2024-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Biomedical and environmental sciences : BES","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.3967/bes2024.041","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}

引用次数: 0

Abstract

Objective: This study aimed to clarify the intervention effect of salidroside (SAL) on lung injury caused by PM _2.5 in mice and illuminate the function of SIRT1-PGC-1ɑ axis.

Methods: Specific pathogen-free (SPF) grade male C57BL/6 mice were randomly assigned to the following groups: control group, SAL group, PM _2.5 group, SAL+PM _2.5 group. On the first day, SAL was given by gavage, and on the second day, PM _2.5 suspension was given by intratracheal instillation. The whole experiment consist of a total of 10 cycles, lasting 20 days. At the end of treatment, blood samples and lung tissues were collected and analyzed. Observation of pathological changes in lung tissue using inverted microscopy and transmission electron microscopy. The expression of inflammatory, antioxidants, apoptosis, and SIRT1-PGC-1ɑ proteins were detected by Western blotting.

Results: Exposure to PM _2.5 leads to obvious morphological and pathologica changes in the lung of mice. PM _2.5 caused a decline in levels of antioxidant-related enzymes and protein expressions of HO-1, Nrf2, SOD2, SIRT1 and PGC-1ɑ, and an increase in the protein expressions of IL-6, IL-1β, Bax, caspase-9 and cleaved caspase-3. However, SAL reversed the aforementioned changes caused by PM _2.5 by activating the SIRT1-PGC-1α pathway.

Conclusion: SAL can activate SIRT1-PGC-1ɑ to ameliorate PM _2.5-induced lung injury.

查看原文

微信好友朋友圈 QQ好友复制链接

本刊更多论文

水杨甙通过调节小鼠体内的SIRT1-PGC-1α改善PM 2.5诱发的肺损伤

研究目的本研究旨在阐明丹参皂甙（SAL）对PM 2.5所致小鼠肺损伤的干预作用，并阐明SIRT1-PGC-1ɑ轴的功能：将无特定病原体（SPF）级雄性C57BL/6小鼠随机分为以下几组：对照组、SAL组、PM 2.5组、SAL+PM 2.5组。第一天给小鼠灌胃 SAL，第二天给小鼠气管内灌注 PM 2.5 悬浮液。整个实验共 10 个周期，持续 20 天。治疗结束后，收集血液样本和肺组织并进行分析。使用倒置显微镜和透射电子显微镜观察肺组织的病理变化。用 Western 印迹法检测炎症蛋白、抗氧化蛋白、细胞凋亡蛋白和 SIRT1-PGC-1ɑ 蛋白的表达：结果：暴露于 PM 2.5 会导致小鼠肺部发生明显的形态学和病理学变化。PM2.5导致抗氧化相关酶水平下降，HO-1、Nrf2、SOD2、SIRT1和PGC-1ɑ蛋白表达量减少，IL-6、IL-1β、Bax、caspase-9和裂解caspase-3蛋白表达量增加。然而，SAL通过激活SIRT1-PGC-1α通路逆转了PM 2.5引起的上述变化：结论：SAL能激活SIRT1-PGC-1ɑ，从而改善PM 2.5引起的肺损伤。

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分钟内获得全文去求助

来源期刊

Biomedical and environmental sciences : BES

自引率

0.00%

发文量