Alantolactone Alleviates Rise in Markers of Periodontitis by Lipopolysaccharide in Human Periodontal Ligament Cells

Abstract

Alantolactone, a natural sesquiterpene lactone, exerts its antiallergic, antibacterial, antimicrobial, antifungal, anticancer, and neuroprotective effects by virtue of its anti-inflammatory and antioxidant properties. We have extended these observations by examining its effect on markers of periodontitis in lipopolysaccharide treated human periodontal ligament cells. Treatment with lipopolysaccharide induced increase in cell apoptosis and decrease in cell viability that were decreased by alantolactone. Also, alantolactone suppressed lipopolysaccharide induced oxidative stress through upregulation of superoxide dismutase and reduced glutathione and downregulation of malondialdehyde and myeloperoxidase. Moreover, lipopolysaccharideinduced upregulation of tumor necrosis factor-α, interleukin-1β, and interleukin-6 in human periodontal ligament cells was also reduced by alantolactone. Moreover, alantolactone attenuated lipopolysaccharide-induced increase in osteoclast markers, receptor activator of nuclear factor-kappa B ligand, nuclear factor of activated T cells c1, dendritic cell-specific transmembrane protein, and cellular proto-oncogene Fos in RAW 264.7. The increased number of tartrate resistant acid phosphatase-positive RAW 264.7 was also reduced by alantolactone. Finally, alantolactone downregulated levels of p-p65, p-protein kinase, and p-Phosphatidylinositol 3-kinase in lipopolysaccharide treated human periodontal ligament cells. In conclusion, alantolactone reduced osteoclast formation, exerts antioxidant and anti-inflammatory effects in lipopolysaccharide induced human periodontal ligament cells through inactivation of Akt and nuclear factor-kappa B pathways.