| Background:Inflammatory mediators play an important role in periodontitis. Most destruction of periodontal tissues is caused by destructive enzymes in the host, such as matrix metalloproteinases(MMPs) and inflammatory mediators(prostaglandins and interleukins). Primary mediators such as IL-1β and TNF-α induce the production of secondary mediators such as chemokines and prostaglandins,resulting in the amplification of the inflammatory response and leading to the destruction of connective tissue and bone resorption.Adiponectin is a kind of adipocytokines derived from adipocytes and may function as the only negative regulator of obesity in many physiological and pathological processes. This kind of adipocyte-derived hormone was revealed to have anti-inflammatory properties and the functions of Protecting the cardiovascular, increase insulin sensitivity.and have Multiple protective effect to organs. The effects of adiponectin are mediated by being binded to its receptors(ADPR1 and ADPR2). ADPR1 and ADPR2 are expressed in in almost all tissues. The reduction of adiponectin functions may aggravate the progress of periodontitis.The peroxisome proliferator-activated receptor-γ(PPAR-γ) receptor belong to the type II nuclear hormone receptor superfamily. Research show that PPAR-γ agonist was found to have the Potential to regulate cellular inflammatory responses and immune responses. PPAR-γ may play an important role in down-regulatethe level of inflammation, especially in regulating the production of inflammatory mediators,The expression of ADPR1 and ADPR2 may be induced by PPAR-γ in human macrophages. Howerver the influence PPAR-γ signal path have on adiponectin function and related molecular mechanisms remain unknown. Objective:The aim of this study was to explore the change of levels of plasma ADP concentration,levels of ADPR1 and ADPR2 mRNA in experimental periodontitis in rats, evaluate the effect of rosiglitazone on adiponectin receptors(ADPR1, ADPR2)mRNA in gingival tissue,inflammatory factors and the potential of reducing the bone loss in a an experimental periodontitis model. Methods: Fifty famale Sprague-Dawley rats were randomly and equally divided into five groups:Control group;Periodontitis group;Rosiglitazone low dose treatment group;Rosiglitazone median dose treatment group;Rosiglitazone high dose treatment group. Experimental periodontitis model was established by using 0.2mm orthodontic wires, Different concentration of rosiglitazone(1mg/kg,3mg/kg,10mg/kg) was administrated to three rosiglitazone treatment groups for 4 weeks. RT-PCR was used to analyze the expression of ADPR1 mRNA and ADPR2 mRNA in gingiva tissue. Levels of gingival TNF-α,MMP-9 and plasma ADP was measured by ELISA. CEJ-A was measured to evaluate alveolar bone loss by standard digital photographs. Results:The expression levels of gingival ADPR1 mRNA and ADPR2 mRNA in periodontitis group is lower than that in control group(P<0.01). The concen tration of plasma ADP had no significant difference between control group and periodontitis group(P>0.05). The concentration of gingival TNF-α,MMP-9 in periodontitis group was significantly higher than that in in control group(P<0.01). Compared with periodontitis group,all dose of rosiglitazone treatment in creased the expression levels of ADPR1 mRNA(P<0.05)and decreased the c oncentration of TNF-α in gingival tissue. Median and high dose treatment incr eased the expression levels of ADPR2(P<0.01)and concentration of plasma ADP(P<0.05),decreased the concentration of MMP-9 in gingival tissue(P<0.01)and the alveolar bone loss on buccal and palatal side(P<0.01). Conclusions:Adiponectin resistance exists in experimental periodontitis in rats. Rosiglita zone treatment reduced inflammatory response,adiponectinresistance and suppressed the bone resorption probably through up-regulating serum ADP concentrati on,expression levels of ADPRs,and decreasing the concentration of TNF-α,MMP-9 in gingival tissue. |
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