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Arch Oral Biol. 2015 Sep;60(9):1327-32. doi: 10.1016/j.archoralbio.2015.05.005. Epub 2015 May 22.

Tormentic acid inhibits LPS-induced inflammatory response in human gingival fibroblasts via inhibition of TLR4-mediated NF-κB and MAPK signalling pathway.

Author information

1
Department of Stomatolog, PLA General Hospital of Chengdu Military Region, Chengdu 610083, Sichuan Province, PR China; Chengdu Military Garrison Center for Disease Control and Prevention, Chengdu 650032, Sichuan, PR China.
2
Department of Stomatolog, PLA General Hospital of Chengdu Military Region, Chengdu 610083, Sichuan Province, PR China.
3
Chengdu Military Garrison Center for Disease Control and Prevention, Chengdu 650032, Sichuan, PR China.
4
Department of Stomatolog, PLA General Hospital of Chengdu Military Region, Chengdu 610083, Sichuan Province, PR China. Electronic address: lichenjungz@163.com.

Abstract

OBJECTIVE:

Periodontal disease is one of the most prevalent oral diseases, which is associated with inflammation of the tooth-supporting tissues. Tormentic acid (TA), a triterpene isolated from Rosa rugosa, has been reported to exert anti-inflammatory effects. The aim of this study was to investigate the anti-inflammatory effects of TA on lipopolysaccharide (LPS)-stimulated human gingival fibroblasts (HGFs).

METHODS:

The levels of inflammatory cytokines such as interleukin (IL)-6 and chemokines such as IL-8 were detected by enzyme-linked immunosorbent assay (ELISA). The expression of Toll-like receptor 4 (TLR4), nuclear factor kappa B (NF-κB), IκBα, p38, extracellular signal-regulated kinase (ERK), and c-Jun N-terminal kinase (JNK) was determined by Western blotting.

RESULTS:

The results showed that Porphyromonas gingivalis LPS significantly upregulated the expression of IL-6 and IL-8. TA inhibited the LPS-induced production of IL-6 and IL-8 in a dose-dependent manner. Furthermore, TA inhibited LPS-induced TLR4 expression; NF-κB activation; IκBα degradation; and phosphorylation of ERK, JNK, and P38.

CONCLUSION:

TA inhibits the LPS-induced inflammatory response in HGFs by suppressing the TLR4-mediated NF-κB and mitogen-activated protein kinase (MAPK) signalling pathway.

KEYWORDS:

Cytokine; Human gingival fibroblasts; MAPKs; NF-κB; Tormentic acid

[Indexed for MEDLINE]

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