{"title":"The therapeutic potential of Laggera alata in alleviating inflammation and oxidative stress: insights into the miR-150-5p/TRIM8 axis","authors":"JiangCun Wei, Sen Liang, Peng Yang, Bing Qing, JiaBao Ma, LeiMin Jiang, QingMei Deng, Wen Zhong, MingGang Wang, ZuJie Qin","doi":"10.1007/s13273-024-00468-0","DOIUrl":null,"url":null,"abstract":"<h3 data-test=\"abstract-sub-heading\">Objective</h3><p>This research was conducted to study the protective effect of <i>Laggera alata</i> (TPLA) on sepsis-induced liver injury (SLI).</p><h3 data-test=\"abstract-sub-heading\">Methods</h3><p>The SLI model was established in rats by cecal ligation and puncture (CLP), and human liver THLE-3 cells were induced by LPS to establish a cellular SLI model. HE staining and TUNEL staining were performed on the liver tissue of SLI rats treated with TPLA. The effects of TPLA on THLE-3 cells were studied using CCK-8, flow cytometry, ELISA, and biochemical analysis. The functional mechanism of TPLA, miR-150-5p, and TRIM8 in SLI was studied.</p><h3 data-test=\"abstract-sub-heading\">Results</h3><p>TPLA treatment improved SLI in CLP rats and LPS-induced human liver THLE-3 cell injury was manifested by liver tissue injury recovery and decreased apoptosis of liver cells. At the same time, inflammation and oxidative stress were also alleviated. miR-150-5p level was reduced in SLI rats and cells, while TPLA pretreatment restored miR-150-5p level. miR-150-5p inhibitors could impair the therapeutic effect of TPLA in THLE-3 cell damage. TRIM8 was a direct target of miR-150-5p, and there was a negative regulatory relationship between the miR-150-5p and TRIM8 mRNA levels. Overexpressing TRIM8 also weakened the therapeutic effect of TPLA on THLE-3 cell damage.</p><h3 data-test=\"abstract-sub-heading\">Conclusion</h3><p>TPLA reduces TRIM8 expression by upregulating miR-150-5p, thereby reducing inflammatory response and oxidative stress, and thus significantly alleviating SLI.</p>","PeriodicalId":18683,"journal":{"name":"Molecular & Cellular Toxicology","volume":"89 1","pages":""},"PeriodicalIF":1.1000,"publicationDate":"2024-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Molecular & Cellular Toxicology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1007/s13273-024-00468-0","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"TOXICOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Objective
This research was conducted to study the protective effect of Laggera alata (TPLA) on sepsis-induced liver injury (SLI).
Methods
The SLI model was established in rats by cecal ligation and puncture (CLP), and human liver THLE-3 cells were induced by LPS to establish a cellular SLI model. HE staining and TUNEL staining were performed on the liver tissue of SLI rats treated with TPLA. The effects of TPLA on THLE-3 cells were studied using CCK-8, flow cytometry, ELISA, and biochemical analysis. The functional mechanism of TPLA, miR-150-5p, and TRIM8 in SLI was studied.
Results
TPLA treatment improved SLI in CLP rats and LPS-induced human liver THLE-3 cell injury was manifested by liver tissue injury recovery and decreased apoptosis of liver cells. At the same time, inflammation and oxidative stress were also alleviated. miR-150-5p level was reduced in SLI rats and cells, while TPLA pretreatment restored miR-150-5p level. miR-150-5p inhibitors could impair the therapeutic effect of TPLA in THLE-3 cell damage. TRIM8 was a direct target of miR-150-5p, and there was a negative regulatory relationship between the miR-150-5p and TRIM8 mRNA levels. Overexpressing TRIM8 also weakened the therapeutic effect of TPLA on THLE-3 cell damage.
Conclusion
TPLA reduces TRIM8 expression by upregulating miR-150-5p, thereby reducing inflammatory response and oxidative stress, and thus significantly alleviating SLI.
期刊介绍:
Molecular & Cellular Toxicology publishes original research and reviews in all areas of the complex interaction between the cell´s genome (the sum of all genes within the chromosome), chemicals in the environment, and disease. Acceptable manuscripts are the ones that deal with some topics of environmental contaminants, including those that lie in the domains of analytical chemistry, biochemistry, pharmacology and toxicology with the aspects of molecular and cellular levels. Emphasis will be placed on toxic effects observed at relevant genomics and proteomics, which have direct impact on drug development, environment health, food safety, preventive medicine, and forensic medicine. The journal is committed to rapid peer review to ensure the publication of highest quality original research and timely news and review articles.