Patchouli alcohol suppresses inflammation and autophagy, and reduces osteoclast formation in periodontitis via regulation of ERK and NF κB signaling pathways

Abstract

Purpose: To evaluate the effect of patchouli alcohol (PA) on periodontitis and reveal its possible mechanism.
 Methods: Primary human periodontal membrane cells (PDLC) were isolated and treated with lipopolysaccharide (LPS) to establish a periodontitis model. The MTT, flow cytometry and immunofluorescence assay were used to determine the effect of PA on cell viability and apoptosis in PDLC exposed to LPS. The inflammation status and osteoclast formation were measured using enzyme-linked immunosorbent assay (ELISA) and TRAP staining. Immunoblot assays were performed to analyze the effect of LPS on ERK and NF-κB pathways.
 Results: Patchouli alcohol (PA) improved LPS-induced PDLC growth arrest (p < 0.001). In addition, PA relieved LPS - induced autophagy of PDLCs (p < 0.001). Further data confirmed that PA inhibited lPS-induced inflammation of PDLCs. In addition, PA reduced osteoclast formation, and suppressed inflammation and autophagy, and also reduced osteoclast formation by regulating ERK and NF-κB pathways.
 Conclusion: Patchouli alcohol inhibits inflammation and autophagy, and decreases osteoclast formation in periodontitis via the regulation of ERK and NF-κB signaling pathways. Thus, this compound has potentials for development for the treatment of periodontitis; however, in vivo studies should first be undertaken.