{"title":"黄芩苷通过介导METTL14/SOX6轴减轻lps诱导的急性肺损伤细胞毒性。","authors":"Yuexuan Chen, Yuhai Gu, Zhihan Gao","doi":"10.1097/SHK.0000000000002518","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Baicalin (C21H18O11) is a flavonoid component extracted from scutellaria baicalensis with biological activity in various types of diseases, including acute lung injury (ALI). The relevant mechanism behind baicalin in ALI needs further investigation.</p><p><strong>Methods: </strong>ALI model in vitro was established by lipopolysaccharide (LPS) in WI-38 cells (lung fibroblast). Cell growth was determined via MTT assay and EdU assay. Apoptosis was assessed using flow cytometry, caspase 3 assay and TUNEL assay. Oxidative indicators and inflammatory cytokines were detected by commercial kits. Interaction between methyltransferase-like 14 (METTL14) and SRY-Box Transcription Factor 6 (SOX6) was studied using Methylated RNA Immunoprecipitation (MeRIP) and dual-luciferase reporter assay. RT-qPCR and western blot were applied for examining gene levels.</p><p><strong>Results: </strong>Baicalin enhanced cell growth and reduced apoptosis, oxidative stress, inflammation after ALI was induced by LPS. Downregulation of SOX6 weakened LPS-induced cytotoxicity in WI-38 cells. Baicalin prevented from LPS-induced lung cell injury via reducing SOX6 expression. SOX6 expression was stabilized by METTL14 through its methylation modification. METTL14/SOX6 axis was related to the regulation of baicalin in LPS-treated WI-38 cells.</p><p><strong>Conclusion: </strong>Therefore, baicalin played an important role to inhibit LPS-induced cytotoxicity in vitro via METTL14-mediated methylation of SOX6.</p>","PeriodicalId":21667,"journal":{"name":"SHOCK","volume":" ","pages":""},"PeriodicalIF":2.7000,"publicationDate":"2024-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Baicalin alleviates LPS-induced cytotoxicity in acute lung injury through mediating METTL14/SOX6 axis.\",\"authors\":\"Yuexuan Chen, Yuhai Gu, Zhihan Gao\",\"doi\":\"10.1097/SHK.0000000000002518\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>Baicalin (C21H18O11) is a flavonoid component extracted from scutellaria baicalensis with biological activity in various types of diseases, including acute lung injury (ALI). The relevant mechanism behind baicalin in ALI needs further investigation.</p><p><strong>Methods: </strong>ALI model in vitro was established by lipopolysaccharide (LPS) in WI-38 cells (lung fibroblast). Cell growth was determined via MTT assay and EdU assay. Apoptosis was assessed using flow cytometry, caspase 3 assay and TUNEL assay. Oxidative indicators and inflammatory cytokines were detected by commercial kits. Interaction between methyltransferase-like 14 (METTL14) and SRY-Box Transcription Factor 6 (SOX6) was studied using Methylated RNA Immunoprecipitation (MeRIP) and dual-luciferase reporter assay. RT-qPCR and western blot were applied for examining gene levels.</p><p><strong>Results: </strong>Baicalin enhanced cell growth and reduced apoptosis, oxidative stress, inflammation after ALI was induced by LPS. Downregulation of SOX6 weakened LPS-induced cytotoxicity in WI-38 cells. Baicalin prevented from LPS-induced lung cell injury via reducing SOX6 expression. SOX6 expression was stabilized by METTL14 through its methylation modification. METTL14/SOX6 axis was related to the regulation of baicalin in LPS-treated WI-38 cells.</p><p><strong>Conclusion: </strong>Therefore, baicalin played an important role to inhibit LPS-induced cytotoxicity in vitro via METTL14-mediated methylation of SOX6.</p>\",\"PeriodicalId\":21667,\"journal\":{\"name\":\"SHOCK\",\"volume\":\" \",\"pages\":\"\"},\"PeriodicalIF\":2.7000,\"publicationDate\":\"2024-11-21\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"SHOCK\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1097/SHK.0000000000002518\",\"RegionNum\":3,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"CRITICAL CARE MEDICINE\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"SHOCK","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1097/SHK.0000000000002518","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"CRITICAL CARE MEDICINE","Score":null,"Total":0}
Baicalin alleviates LPS-induced cytotoxicity in acute lung injury through mediating METTL14/SOX6 axis.
Background: Baicalin (C21H18O11) is a flavonoid component extracted from scutellaria baicalensis with biological activity in various types of diseases, including acute lung injury (ALI). The relevant mechanism behind baicalin in ALI needs further investigation.
Methods: ALI model in vitro was established by lipopolysaccharide (LPS) in WI-38 cells (lung fibroblast). Cell growth was determined via MTT assay and EdU assay. Apoptosis was assessed using flow cytometry, caspase 3 assay and TUNEL assay. Oxidative indicators and inflammatory cytokines were detected by commercial kits. Interaction between methyltransferase-like 14 (METTL14) and SRY-Box Transcription Factor 6 (SOX6) was studied using Methylated RNA Immunoprecipitation (MeRIP) and dual-luciferase reporter assay. RT-qPCR and western blot were applied for examining gene levels.
Results: Baicalin enhanced cell growth and reduced apoptosis, oxidative stress, inflammation after ALI was induced by LPS. Downregulation of SOX6 weakened LPS-induced cytotoxicity in WI-38 cells. Baicalin prevented from LPS-induced lung cell injury via reducing SOX6 expression. SOX6 expression was stabilized by METTL14 through its methylation modification. METTL14/SOX6 axis was related to the regulation of baicalin in LPS-treated WI-38 cells.
Conclusion: Therefore, baicalin played an important role to inhibit LPS-induced cytotoxicity in vitro via METTL14-mediated methylation of SOX6.
期刊介绍：
SHOCK®: Injury, Inflammation, and Sepsis: Laboratory and Clinical Approaches includes studies of novel therapeutic approaches, such as immunomodulation, gene therapy, nutrition, and others. The mission of the Journal is to foster and promote multidisciplinary studies, both experimental and clinical in nature, that critically examine the etiology, mechanisms and novel therapeutics of shock-related pathophysiological conditions. Its purpose is to excel as a vehicle for timely publication in the areas of basic and clinical studies of shock, trauma, sepsis, inflammation, ischemia, and related pathobiological states, with particular emphasis on the biologic mechanisms that determine the response to such injury. Making such information available will ultimately facilitate improved care of the traumatized or septic individual.
京公网安备 11010802042870号
京ICP备2023020795号-1
分享
求助内容：
应助结果提醒方式：
扫码关注我们
