Article Publish Status: FREE
Abstract Title:

Baicalin inhibits LPS-induced inflammation in RAW264.7 cells through miR-181b/HMGB1/TRL4/NF-κB pathway.

Abstract Source:

Am J Transl Res. 2021 ;13(9):10127-10141. Epub 2021 Sep 15. PMID: 34650685

Abstract Author(s):

Guoliang Yan, Liyun Chen, Haihui Wang, Sai Wu, Shufang Li, Xinlu Wang

Article Affiliation:

Guoliang Yan


PURPOSE: Inflammation out of control may induce many diseases. Baicalin has certain anti-inflammatory effects, but its mechanism of action is not clear. Therefore, this study was designed to explore a potential mechanism of anti-inflammation.

METHODS: In this study, RAW264.7 cells were induced by 1.0 g/mL lipopolysaccharide (LPS) and then exposed to baicalin at various concentrations (0.1-1.0μmol/L). Then, we investigated the effect of baicalin in RAW264.7 inflammation models.

RESULTS: In this study, 0.1-1.0μmol/L baicalin, especially baicalin at 1.0 μmol/L, effectively inhibited the expression of inflammatory factors (TNF-α, IL-1β, IL-6, Cox, and iNOS), decreased the activity of High Mobility Group Box 1 (HMGB1)/Toll-like Receptor 4 (TLR4)/nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) pathway, and stimulated miR-181b expression. HMGB1 was proved to be negatively regulated by miR-181b. Here, up-regulation of miR-181b or down-regulation of HMGB1 exerted similar effects as baicalin and down-regulated miR-181b reversed the anti-inflammatory effect of baicalin in RAW264.7 inflammation models.

CONCLUSION: Baicalin can inhibit LPS-induced inflammation in RAW264.7 cells via the miR-181b/HMGB1/TRL4/NF-κB pathway.

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