Baicalin attenuates LPS-induced periodontal inflammation response by inhibiting autophagy

BA significantly reduced lipopolysaccharide induced inflammatory responses in PDLCs, as evidenced by a decrease in the levels of inflammatory cytokines. RNA Seq analysis indicated that these effects were associated with autophagy related processes. Notably, BA decreased Beclin levels, reduced the LC3B, diminished LC3B protein staining, and decreased the number of autophagosomes. Furthermore, BA triggered the activation of the PI3K, AKT, mTOR pathway, demonstrated by the increased phosphorylation of these proteins. BA acts as a protective agent against LPS induced periodontal inflammation by modulating autophagy, positioning it as a promising candidate for future periodontal therapies.