| Periodontitis is initiated by an overgrowth of specific gram-negative anaerobic bacteria, but it occurs in only a subset of the population, because it is also influenced by the individual’s immune response and genetic state. Periodontitis involves the destruction of the supporting structures of the teeth including the periodontal ligament, bone and soft tissues. So periodontitis leads to gingival connective tissue destruction, irreversible alveolar bone resorption and tooth loss. Periodontitis is modified by several factors such as smoking, certain drugs, systemic disease and hormonal changes that occur in puberty and pregnancy.Porphyromonas gingivalis, a Gram-negative bacterium, is strongly related with the onset of periodontitis. P. gingivalis lipopolysaccharides are considered to be key factors in the development of chronic periodontitis. Lipopolysaccharide induction of disease leads to the initiation of a local host response in gingival tissues that involves recruitment of inflammatory cells, generation of prostanoids and cytokines, elaboration of lytic enzymes and activation of osteoclasts. Porphyromonas gingivalis lipopolysaccharide preferentially utilizes toll-like receptor-2 and not toll-like receptor-4. Earlier data indicated that P. gingivalis lipopolysaccharide bound toll-like receptor-4 in gingival fibroblasts. Regardless of which toll-like receptor is engaged, lipopolysaccharide increases osteoblastic expression of RANKL, interleukin-1, interleukin-8, prostaglandin E2 and tumor necrosis factor-a, each known to induce osteoclast activity, viability and differentiation.Periodontitis is a chronic inflammatory disease, numerous studies show that high levels of Thl/Th2 cytokine profiles present in the tissue of periodontitis. Still another researches found that the stable lesion is mediated by Thl cells and the progressive lesion by Th2 cells. The control of Thl/Th2 cytokine profiles is therefore fundamental in determining the ultimate outcome of chronic periodontitis.Recently, active compounds endowed with a capacity to modulate the host inflammatory response have received considerable attention as they may represent potential new therapeutic agents for treating periodontal diseases. Curcumin (diferuloylmethane), a polyphenol, is an active principle of the perennial herb Curcuma longa (commonly known as turmeric). Throughout the Orient, it has traditionally been used to good therapeutic effect, particularly as an anti-inflammatory, and many of its therapeutic effects have been confirmed by modern scientific research. Such effects include antioxidant, anti-inflammatory, anticarcinogenic and antimicrobial, hepatoprotective, cardiovascular, hypoglycemic, and antiarthritic.Methods:1. RAW264.7 cells treated with P. gingivalis LPS for 6h, TNF-a and IL-1βexpressions were separately detected by RT-PCR and ELISA. Next, activation of NF-KB-dependent transcription was examined by Immunofluorescent staining and luciferase assay.2. RAW264.7 cells pre-treated with various concentrations of curcumin were stimulated by P. gingivalis LPS. TNF-αand IL-1βexpressions were separately detected by RT-PCR and ELISA. Next, the activation of NF-KB-dependent transcription was examined by luciferase assay.Results:1. RT-PCR and ELISA show that RAW264.7 cells weakly expressed the TNF-a under the control condition, while IL-1βgene was not detected; however, both of them increased following stimulation with P. gingivalis LPS.2. It was observed that treatment with 5,10,20 and 30μM curcumin did not significantly affect the viability of RAW264.7 cells. Curcumin dose-dependently inhibited TNF-αand IL-1βgene expression and protein synthesis in RAW264.7 cells stimulated with P. gingivalis LPS. P. gingivalis LPS activated NF-κB Bdependent transcription in RAW264.7 cells, which were down-regulated by pre-treatment with curcumin as well.Conclusion:Our data suggest that curcumin can inhibit P. gingivalis LPS-induced cytokine expression, and that this could be due to the inhibition of the NF-κB pathway. |
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