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目的 观察缬草油对2型糖尿病大鼠肾脏的保护作用并探讨其机制。方法 将实验动物分为正常对照组、糖尿病组、缬草油组及厄贝沙坦组。检测各组喂养4周、5周、11周、17周的血糖、血胰岛素、血甘油三酯(TG)、血胆固醇(TC)水平;喂养11周、17周的血肌酐(Scr)、血尿素氮(BUN)、尿白蛋白排泄率(UAE)、肾组织中丙二醛(MDA)含量、铜锌超氧化物歧化酶(Cu-Zn SOD)、过氧化氢酶(CAT)、谷胱甘肽过氧化酶(GSH-Px)及蛋白激酶C(PKC)活性,同时留取肾脏作HE染色行病理检查。结果 与糖尿病组相比,缬草油组血TG、TC、Scr、BUN、UAE、肾脏MDA含量、肾细胞膜PKC均明显下降,而肾脏抗氧化酶活性,包括Cu-Zn SOD、CAT、GSH-PX,则明显上升。病理检查发现缬草油组较糖尿病组肾小球体积稍缩小,系膜增生明显减轻。治疗后缬草油组与厄贝沙坦组相比,Scr、BUN、UAE的下降及肾脏病理改变的改善无明显差异。结论 缬草油可以明显改善2型糖尿病大鼠的肾脏损害,减少蛋白尿,延缓肾功能损害的进展。其作用与其降低血脂、抗氧化、抑制肾皮质内PKC的激活有关。
Objective To observe the protective effect of valerian oil on type 2 diabetic rat kidney and to explore its mechanism. Methods The experimental animals were divided into normal control group, diabetic group, valerian oil group and irbesartan group. Blood glucose, blood insulin, blood triglyceride (TG) and blood cholesterol (TC) levels were measured at 4 weeks, 5 weeks, 11 weeks, and 17 weeks in each group; serum creatinine (Scr) and blood were fed for 11 weeks and 17 weeks. Urea nitrogen (BUN), urinary albumin excretion rate (UAE), malondialdehyde (MDA) content in kidney tissue, copper-zinc superoxide dismutase (Cu-Zn SOD), catalase (CAT), and glutathione Glycoperoxidase (GSH-Px) and protein kinase C (PKC) activity were also obtained, and kidneys were taken for HE staining for pathological examination. Results Compared with diabetic group, blood TG, TC, Scr, BUN, UAE, MDA content in kidney, PKC of renal cell membrane in valerian oil group were all significantly decreased, and renal antioxidant enzyme activity including Cu-Zn SOD, CAT, GSH- PX is obviously rising. Pathological examination showed that the glomeruli volume in the valerian oil group was slightly smaller than that in the diabetic group, and mesangial hyperplasia was significantly reduced. After treatment, the decrease of Scr, BUN and UAE and the improvement of pathological changes of kidney were not significantly different between the valerian oil group and the irbesartan group. Conclusion Valerian oil can significantly improve renal damage in type 2 diabetic rats, reduce proteinuria, and delay the progression of renal impairment. Its role is related to its reduction of blood lipids, anti-oxidation, and inhibition of PKC activation in the renal cortex.