Asiatic acid inhibits LPS-induced inflammatory response in human gingival fibroblasts

• Published in: International immunopharmacology 2017-09, Vol.50, p.313-318
• Main Authors: Hao, Chunbo, Wu, Buling, Hou, Zhiming, Xie, Qi, Liao, Tianan, Wang, Tao, Ma, Dandan
• Format: Article
• Language: English
• Subjects: Acids; Anilides - pharmacology; Animals; Anti-Inflammatory Agents - pharmacology; Antioxidants; Asiatic acid; Centella - immunology; Dinoprostone - metabolism; Enzyme-linked immunosorbent assay; Fibroblasts; Fibroblasts - drug effects; Fibroblasts - immunology; Fibroblasts - pathology; Gingiva - pathology; Gingivitis - drug therapy; Human behavior; Human gingival fibroblasts; Humans; In vivo methods and tests; Inflammation; Inflammatory response; Interleukin 6; Interleukin 8; Lipopolysaccharides; Lipopolysaccharides - immunology; LPS; Macrophages - drug effects; Macrophages - immunology; Male; Mice; NF-kappa B - metabolism; NF-κB protein; Nitric Oxide - metabolism; Oral diseases; Pentacyclic Triterpenes - pharmacology; Periodontitis; Peroxisome proliferator-activated receptors; Phosphorylation; PPAR gamma - antagonists & inhibitors; PPAR gamma - metabolism; PPAR-γ; Prostaglandin E2; Protein expression; Rats; Rats, Sprague-Dawley; RAW 264.7 Cells; Tissues
• ISSN: 1567-5769; 1878-1705
• DOI: 10.1016/j.intimp.2017.07.005

Asiatic acid, a triterpenoid component isolated from Centella asiatica (L.) Urban, possesses antioxidative and anti-inflammatory activities. In this study, we aimed to investigate the anti-inflammatory effects of asiatic acid both in vivo and in vitro. HGFs or RAW264.7 cells were treated with asiatic acid 1h before LPS treatment. Cell viability was measured by MTT assay. The levels of PGE2, NO, IL-6, and IL-8 were detected by ELISA. Protein expression levels were detected by western blot analysis. In vivo, asiatic acid significantly inhibited LPS-induced IL-6 and IL-8 expression levels in gingival tissues. In vitro, LPS-induced PGE2, NO, IL-6, and IL-8 production was significantly attenuated by asiatic acid. Asiatic acid also inhibited p65 NF-κB phosphorylation induced by LPS in HGFs. The expression of PPAR-γ was up-regulated by asiatic acid. Furthermore, GW9662, a PPAR-γ inhibitor, attenuated the inhibitory effect of asiatic acid on PGE2, NO, IL-6, and IL-8 production. Our results suggest that asiatic acid activates PPAR-γ, which subsequently inhibits LPS-induced NF-κB activation and inflammatory mediators production. Asiatic acid may offer therapeutic potential for the treatment of periodontitis. •LPS-induced PGE2, NO, IL-6, and IL-8 production were significantly attenuated by asiatic acid.•Asiatic acid also inhibited p65 NF-κB phosphorylation induced by LPS in HGFs.•The expression of PPAR-γ was up-regulated by treatment of asiatic acid.•GW9662 attenuated the inhibition of asiatic acid on PGE2, NO, IL-6, and IL-8 production.