Salvianolic Acid A Attenuates Lipopolysaccharide-Induced Acute Lung Injury by Activating AMPK/SIRT1/Nrf2 Signaling Pathway

IF 3.2 3区医学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY

Journal of Biochemical and Molecular Toxicology Pub Date : 2025-04-24 DOI:10.1002/jbt.70282

Pengwei Wang, Yu Sun, Ru Zhang, Yongli Guo, Yongheng Zhang, Shengjie Guo, Yemin Wang, Jianlian Gao, Pengfei Yang, Zhijian Deng

{"title":"Salvianolic Acid A Attenuates Lipopolysaccharide-Induced Acute Lung Injury by Activating AMPK/SIRT1/Nrf2 Signaling Pathway","authors":"Pengwei Wang, Yu Sun, Ru Zhang, Yongli Guo, Yongheng Zhang, Shengjie Guo, Yemin Wang, Jianlian Gao, Pengfei Yang, Zhijian Deng","doi":"10.1002/jbt.70282","DOIUrl":null,"url":null,"abstract":"<div>\n \n <p>Salvianolic acid A (Sal A) has been reported to have anti-inflammatory and antioxidant properties. The present study aimed to explore the potential mechanisms of Sal A on lipopolysaccharide (LPS)-induced acute lung injury (ALI). The results indicated that Sal A pretreatment attenuated LPS induced lung injury, shown by alleviated histopathological damage and alveolar-capillary barrier dysfunction, as well as reduced inflammatory response and oxidative stress. Moreover, Sal A pretreatment effectively increased the expression of p-AMPK and SIRT1 and promoted Nrf2 nuclear translocation in lung tissues. However, these effects were remarkably blunted by Compound C. Molecular docking experiments further confirmed that Sal A bound well to the active sites of AMPK and SIRT1. In conclusion, these results indicated that Sal A exerted its protective effects on LPS-induced ALI through suppressing inflammation and oxidative stress, which was mainly dependent on the activation of AMPK/SIRT1/Nrf2 signaling pathway.</p></div>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"39 5","pages":""},"PeriodicalIF":3.2000,"publicationDate":"2025-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Biochemical and Molecular Toxicology","FirstCategoryId":"3","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1002/jbt.70282","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}

引用次数: 0

Abstract

Salvianolic acid A (Sal A) has been reported to have anti-inflammatory and antioxidant properties. The present study aimed to explore the potential mechanisms of Sal A on lipopolysaccharide (LPS)-induced acute lung injury (ALI). The results indicated that Sal A pretreatment attenuated LPS induced lung injury, shown by alleviated histopathological damage and alveolar-capillary barrier dysfunction, as well as reduced inflammatory response and oxidative stress. Moreover, Sal A pretreatment effectively increased the expression of p-AMPK and SIRT1 and promoted Nrf2 nuclear translocation in lung tissues. However, these effects were remarkably blunted by Compound C. Molecular docking experiments further confirmed that Sal A bound well to the active sites of AMPK and SIRT1. In conclusion, these results indicated that Sal A exerted its protective effects on LPS-induced ALI through suppressing inflammation and oxidative stress, which was mainly dependent on the activation of AMPK/SIRT1/Nrf2 signaling pathway.

查看原文本刊更多论文

丹酚酸A通过激活AMPK/SIRT1/Nrf2信号通路减轻脂多糖诱导的急性肺损伤

据报道，丹酚酸A （Salvianolic acid A, Sal A）具有抗炎和抗氧化特性。本研究旨在探讨Sal A在脂多糖（LPS）诱导的急性肺损伤（ALI）中的作用机制。结果表明，Sal A预处理可减轻LPS诱导的肺损伤，表现为减轻组织病理损伤和肺泡-毛细血管屏障功能障碍，减轻炎症反应和氧化应激。此外，Sal A预处理可有效提高p-AMPK和SIRT1的表达，促进Nrf2在肺组织中的核易位。分子对接实验进一步证实，Sal A与AMPK和SIRT1活性位点结合良好。综上所述，这些结果表明，Sal A对lps诱导的ALI的保护作用主要通过抑制炎症和氧化应激发挥，其保护作用主要依赖于AMPK/SIRT1/Nrf2信号通路的激活。

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

Journal of Biochemical and Molecular Toxicology 生物-毒理学

CiteScore

5.80

自引率

2.80%

发文量

277

审稿时长

6-12 weeks

期刊介绍： The Journal of Biochemical and Molecular Toxicology is an international journal that contains original research papers, rapid communications, mini-reviews, and book reviews, all focusing on the molecular mechanisms of action and detoxication of exogenous and endogenous chemicals and toxic agents. The scope includes effects on the organism at all stages of development, on organ systems, tissues, and cells as well as on enzymes, receptors, hormones, and genes. The biochemical and molecular aspects of uptake, transport, storage, excretion, lactivation and detoxication of drugs, agricultural, industrial and environmental chemicals, natural products and food additives are all subjects suitable for publication. Of particular interest are aspects of molecular biology related to biochemical toxicology. These include studies of the expression of genes related to detoxication and activation enzymes, toxicants with modes of action involving effects on nucleic acids, gene expression and protein synthesis, and the toxicity of products derived from biotechnology.