Baicalein induces apoptosis and reduces inflammation in LPS-stimulated keratinocytes by blocking the activation of NF-kappaB: implications for alleviating oral lichen planus.

ic inflammatory diseases, including OLP, involves in the activation of the nuclear factor-kappa B (NF-kappaB) signaling pathway. Baicalein (BAI) is an alcohol soluble flavonoid known for its anti-inflammatory effect. However, its effectiveness on keratinocytes in OLP remains unclear. In the present study, we examined inflammation in oral mucosa tissue from OLP patients. Hematoxylin and eosin staining showed denser subepithelial lymphocytes infiltration compared to the normal oral mucosa epithelium. TNF-alpha and IL-6 were up-regulated in oral mucosa tissue of OLP patients. We next stimulated humans keratinocytes (HaCaT cells) with lipopolysaccharide (LPS) to create an inflammatory environment like that in the OLP tissue and assessed the effect of BAI on OLP and NF-kappaB signaling pathways. Our results showed that BAI treatment inhibited the level of TNF-alpha and IL-6 induced by LPS. However, the cells apoptosis was promoted after BAI treatment. Furthermore, BAI not only inhibited LPS-induced p38 MAPK and ERK1/2 phosphorylation, but also NF-kappaB activation by reducing IkappaBalpha phosphorylation and the nuclear translocation of NFkappaB-p65 and NFkappaB-p50 from cytoplasm to nucleus in keratinocytes. Our findings suggest that BAI inhibits the production of inflammatory cytokines by negatively regulating the NF-kappaB signaling pathway under LPS simulation in HaCaT cells.