Our study investigated the effects of
acacetin, a natural
flavonoid compound, on the survival and expression of inflammatory related
cytokines in
lipopolysaccharide (LPS)-stimulated human periodontal ligament (PDL) cells. Treatment with
acacetin significantly promoted survival and suppressed apoptosis in LPS-stimulated PDL cells in a dose-dependent manner, as shown by
CCK-8 and flow cytometry assays, respectively. Moreover, ELISA assay showed that
acacetin dose-dependently attenuated LPS-induced increases of TNF-α,
IL-6 and IL-1β in PDL cells. Western blot analysis showed that administration of
acacetin dose-dependently increased the ratio of LC3II/LC3I, as well as the expression of
beclin-1, as compared to LPS-stimulated PDL cells. Inhibition of autophagy by
rapamycin, an autophagy inhibitor, increased the production of pro-inflammatory
cytokines and decreased survival, abolishing the beneficial role of
acacetin in LPS-stimulated PDL cells. In addition, the expression of GSK-3β, a regulator of autophagy, was suppressed by administration with
acacetin in a dose-dependent manner.
Acacetin treatment promotes survival and suppresses
inflammation in LPS-stimulated PDL cells via regulating autophagy and GSK-3β signal in PDL cells, suggesting that
acacetin may be a potential novel agent for the treatment of
chronic periodontitis.