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.
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