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目的探讨PPARγ激活对糖尿病兔骨折愈合的影响。方法选取浙江中医药大学动物实验研究中心2016年6月普通级健康雄性兔18只,随机分成对照组、糖尿病组和PPARγ激活组,各6只。糖尿病组和PPARγ激活组建立高血糖动物模型,3组均建立骨折模型。比较3组空腹血糖(FPG)、三酰甘油(TG)、骨形态发生蛋白2(BMP-2)、转化生长因子β_1(TGF-β_1)、血小板衍生因子(PDGF)、碱性成纤维细胞生长因子(bFGF)水平及体质量。结果给药前,3组兔体质量比较,差异无统计学意义(P>0.05);糖尿病组与PPARγ激活组FPG、TG水平高于对照组(P<0.05),而糖尿病组与PPARγ激活组FPG、TG水平比较,差异无统计学意义(P>0.05)。给药后,糖尿病组、PPARγ激活组体质量低于对照组,FPG、TG水平高于对照组(P<0.05);PPARγ激活组体质量高于糖尿病组,FPG、TG水平低于糖尿病组(P<0.05)。糖尿病组治疗1、2、3周时BMP-2、TGF-β_1、bFGF水平低于对照组,治疗1周时PDGF水平低于对照组(P<0.05);PPARγ激活组治疗1、2、3周时bFGF水平低于糖尿病组,治疗2、3周时BMP-2、TGF-β_1、PDGF水平低于糖尿病组(P<0.05)。结论 PPARγ激活后可造成糖尿病患者骨质流失,不利于骨折的愈合。
Objective To investigate the effect of PPARγ activation on fracture healing in diabetic rabbits. Methods 18 healthy male rabbits of normal grade were selected from Animal Experimental Research Center of Zhejiang University of Chinese Medicine in June 2016 and randomly divided into control group, diabetic group and PPARγ-activated group, each with 6 rats. Diabetic rats and PPARγ activation group established animal model of hyperglycemia, fracture models were established in all three groups. The levels of fasting blood glucose (FPG), triglyceride (TG), bone morphogenetic protein 2 (BMP-2), transforming growth factor beta 1 (TGF-beta 1), platelet derived factor (PDGF) and basic fibroblast growth Factor (bFGF) level and body weight. Results Before treatment, there was no significant difference in the body weight between the three groups (P> 0.05). The levels of FPG and TG in diabetic group and PPARγ-activated group were higher than those in control group (P <0.05), while those in diabetic group and PPARγ-activated group FPG, TG levels, the difference was not statistically significant (P> 0.05). After administration, the quality of diabetic group and PPARγ-activated group was lower than that of the control group, FPG and TG levels were higher than those of the control group (P <0.05); the body mass of PPARγ-activated group was higher than that of diabetic group, FPG and TG were lower than those of diabetic group P <0.05). The levels of BMP-2, TGF-β 1 and bFGF in diabetic group were lower than those in control group at 1, 2, and 3 weeks of treatment, the level of PDGF was lower at 1 week than that of control group (P <0.05) The level of bFGF was lower than that of the diabetic group on week 1, and the levels of BMP-2, TGF-β 1 and PDGF were lower than those of the diabetic group at 2 and 3 weeks (P <0.05). Conclusion PPARγ activation can cause bone loss in patients with diabetes, is not conducive to fracture healing.