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.