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目的:观察缬沙坦对实验性2型糖尿病大鼠肾脏病变的保护作用及其机制。方法:链脲佐菌素(STZ)诱导的糖尿病肾病大鼠模型随机分为对照组糖尿病组及治疗组(缬沙坦10mg·kg~(-1)·d~(-1)),治疗6周后,比较各组大鼠肾组织中丙二醛(MDA)含量和超氧化物歧化酶(SOD)活性,同时检测各组大鼠血糖、血肌酐、尿素氮、24h尿蛋白定量等。采用RT-PCR方法检测P22phoxmRNA表达。结果:治疗组较非治疗组明显改善尿白蛋白、尿素氮水平和肾脏肥大指数。肾脏MDA含量明显下降(P＜0．05),SOD活性显著上升(P＜0．05)。p22phox的mRNA相对含量在糖尿病组为(0．875±0．94),明显高于单切时照组(0．297±0．067)(P＜0．01),在治疗组为(0．484±0．064),较糖尿病组显著降低(P＜0．01),但仍高于对照组(P＜0．05)。结论:缬沙坦对2型糖尿病肾脏病变有一定的保护作用,其机制可能是通过抑制氧化应激反应,下调糖尿病大鼠P22phoxmRNA的表达对2型糖尿痛模型大鼠肾脏产生保护作用。
Objective: To observe the protective effects of valsartan on renal lesions in experimental type 2 diabetic rats and its mechanism. Methods: Rats with diabetic nephropathy induced by streptozotocin (STZ) were randomly divided into diabetic group and control group (valsartan 10 mg · kg -1 · d -1), treatment 6 Afterwards, the content of malondialdehyde (MDA) and the activity of superoxide dismutase (SOD) in renal tissues of rats in each group were compared. The blood glucose, serum creatinine, urea nitrogen and 24 h urinary protein were measured at the same time. P22phox mRNA expression was detected by RT-PCR. Results: Compared with non-treatment group, the treatment group significantly improved urinary albumin, urea nitrogen and renal hypertrophy index. Kidney MDA content decreased significantly (P <0.05), SOD activity increased significantly (P <0.05). The relative mRNA level of p22phox in diabetic group was (0.875 ± 0.94), which was significantly higher than that in monophasic group (0.297 ± 0.067) (P <0.01) .484 ± 0.064), which was significantly lower than that of diabetic group (P <0.01), but still higher than that of control group (P <0.05). CONCLUSION: Valsartan has a protective effect on nephropathy in type 2 diabetic rats. The possible mechanism is that valsartan may have a protective effect on the kidney of type 2 diabetic rats by inhibiting oxidative stress and down-regulating the expression of P22phox mRNA in diabetic rats.