1. Asiatic acid inhibits LPS-induced inflammatory response in human gingival fibroblasts.
- Author
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Hao C, Wu B, Hou Z, Xie Q, Liao T, Wang T, and Ma D
- Subjects
- Anilides pharmacology, Animals, Centella immunology, Dinoprostone metabolism, Fibroblasts drug effects, Fibroblasts pathology, Humans, Lipopolysaccharides immunology, Macrophages drug effects, Male, Mice, NF-kappa B metabolism, Nitric Oxide metabolism, PPAR gamma antagonists & inhibitors, PPAR gamma metabolism, RAW 264.7 Cells, Rats, Rats, Sprague-Dawley, Anti-Inflammatory Agents pharmacology, Fibroblasts immunology, Gingiva pathology, Gingivitis drug therapy, Macrophages immunology, Pentacyclic Triterpenes pharmacology
- Abstract
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., (Copyright © 2017 Elsevier B.V. All rights reserved.)
- Published
- 2017
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