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目的:研究罗格列酮对糖尿病大鼠血清超敏C反应蛋白(hs-CRP)水平的影响及罗格列酮的肾脏保护作用。方法:将45只大鼠随机分为正常对照组(n=15)、糖尿病组(n=15)和罗格列酮组(n=15)。糖尿病大鼠模型建立后,罗格列酮组给予5 mg.kg-1.d-1罗格列酮+生理盐水混悬液灌胃,正常对照组和糖尿病组灌以相应量的生理盐水。分别在处理4、8和12周后观察各组大鼠的血清hs-CRP、尿微量白蛋白(MAU)水平及血糖(BG)、糖化血红蛋白Alc(HbAlc)、尿素氮(BUN)等生化指标变化。结果:糖尿病组与罗格列酮组在第4、8和12周BG、HbAlc、BUN、MAU和hs-CRP表达水平均明显高于正常对照组(P<0.05);罗格列酮组在第8和12周BG、HbAlc、BUN、MAU和hs-CRP表达水平均明显低于糖尿病组(均P<0.05);糖尿病组BG、HbAlc、BUN、MAU和hs-CRP表达水平随时间延长逐渐升高(均P<0.05);罗格列酮组BG、HbAlc、BUN、MAU和hs-CRP表达水平随时间延长逐渐下降(均P<0.05)。hs-CRP与MAU呈显著正相关(r=0.687,P<0.01)。结论:罗格列酮对糖尿病大鼠肾脏具有一定的保护作用,可能与其降低血清hs-CRP的表达水平、减轻炎症反应有关。
Objective: To investigate the effect of rosiglitazone on the serum hs-CRP level in diabetic rats and the protective effect of rosiglitazone on kidney. Methods: Forty five rats were randomly divided into normal control group (n = 15), diabetic group (n = 15) and rosiglitazone group (n = 15). After the diabetic rat model was established, the rosiglitazone group was administered with 5 mg.kg-1.d-1 rosiglitazone + saline suspension. The normal control group and the diabetic group were given the corresponding amount of normal saline. The serum levels of hs-CRP, MAU, blood glucose (BG), HbAlc and BUN were observed at 4, 8 and 12 weeks after treatment respectively. Variety. Results: The expression levels of BG, HbAlc, BUN, MAU and hs-CRP in diabetic group and rosiglitazone group at 4, 8 and 12 weeks were significantly higher than those in normal control group (P <0.05) The expression levels of BG, HbAlc, BUN, MAU and hs-CRP in diabetic group were significantly lower than those in diabetic group at week 8 and 12 (all P <0.05). The expression levels of BG, HbAlc, BUN, MAU and hs-CRP in diabetic group gradually increased with time (All P <0.05). The expression of BG, HbAlc, BUN, MAU and hs-CRP in rosiglitazone group decreased gradually with time (all P <0.05). There was a significant positive correlation between hs-CRP and MAU (r = 0.687, P <0.01). CONCLUSION: Rosiglitazone protects the kidney of diabetic rats to some extent, which may be related to the decrease of serum hs-CRP expression and inflammation.