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

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.

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

In this study, 0.1-1.0 μmol/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.

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