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目的建立Ⅱ型糖尿病大鼠模型,在辅酶Q10干预下,通过酶联免疫吸附实验(ELISA)检测Ⅱ型糖尿病大鼠模型在牙周炎发生过程中血清骨保护素(osteoprotegerin,OPG)、核因子-κB受体活化因子配体(receptor activator for nuclear factor-κB ligand,RANKL)的水平的改变,探讨辅酶Q10在阻断或延缓糖尿病大鼠牙周炎发病进程中的意义。方法选取64只(体质量180~200g)健康Wistar大鼠,随机分4组,每组16只,分别为空白组(O组)、牙周炎组(P组)、糖尿病牙周炎组(DMP组)、辅酶Q10糖尿病牙周炎组(QDMP组)。DMP、QDMP组大鼠高脂高糖饮食4周+低剂量腹腔注射链脲佐菌素(40mg/kg),建立Ⅱ型糖尿病大鼠模型。造模成功后QDMP组大鼠给药至实验结束,其余组大鼠每日给予同剂量生理盐水。在给药第4周末对P、DMP、QDMP组大鼠进行牙周结扎。分别于给药前(糖尿病造模后)和给药后4周(结扎后),8周(结扎后4周),12周(结扎后8周)末处死大鼠每组4只,ELISA法检测大鼠血清OPG、RANKL的水平的改变并进行统计学分析。结果给药12周(结扎后8周)末,辅酶Q10干预组较糖尿病牙周炎组血清OPG、RANKL水平下降(P<0.01),RANKL/OPG比值上升(P<0.05),有统计学意义。结论辅酶Q10对糖尿病大鼠牙周炎的延缓作用有可能是通过调节血清中OPG、RANKL的表达差异来实现的。
Objective To establish a rat model of type Ⅱ diabetes mellitus (T2DM) and detect the expression of serum osteoprotegerin (OPG), nuclear factor kappa B (NF - κB) in type Ⅱ diabetic rat model by enzyme linked immunosorbent assay (ELISA) κB receptor activator of nuclear factor-κB ligand (RANKL), and to explore the significance of coenzyme Q10 in blocking or delaying the onset of periodontitis in diabetic rats. Methods Sixty-four healthy Wistar rats weighing 180-200g were randomly divided into 4 groups (n = 16), which were blank group (O group), periodontitis group (P group), diabetic periodontitis group DMP group) and coenzyme Q10 diabetic periodontitis group (QDMP group). Rats in DMP and QDMP groups were given high-fat and high-sucrose diet for 4 weeks and low-dose streptozotocin (40mg / kg) intraperitoneally to establish type 2 diabetic rat model. After successful modeling, rats in QDMP group were given the drug until the end of the experiment. The rest rats were given the same dose of normal saline daily. Periodontal ligature was performed on rats in P, DMP and QDMP groups at the end of the fourth week. Rats in each group were sacrificed 4 weeks after administration (after modeling of diabetes), 4 weeks after administration (after ligation), 8 weeks (4 weeks after ligation) and 12 weeks (8 weeks after ligation) The levels of serum OPG and RANKL in rats were detected and analyzed statistically. Results Compared with diabetic periodontitis group, the levels of OPG and RANKL in coenzyme Q10 intervention group decreased (P <0.01) and the ratio of RANKL / OPG increased (P <0.05) at the end of 12 weeks after administration (8 weeks after ligation) . Conclusion Delayed effects of coenzyme Q10 on periodontitis in diabetic rats may be achieved by regulating the expression of OPG and RANKL in serum.