BAICALIN ALLEVIATES LPS-INDUCED CYTOTOXICITY IN ACUTE LUNG INJURY THROUGH MEDIATING METTL14/SOX6 AXIS.

Background : Baicalin (C 21 H 18 O 11 ) 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 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 and dual-luciferase reporter assay. Reverse transcription-quantitative polymerase chain reaction and Western blot were applied for examining gene levels. Results : Baicalin enhanced cell growth and reduced apoptosis and 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.