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目的观察贝那普利对阿霉素诱导的SD大鼠肾损伤的保护作用。方法阿霉素诱导SD大鼠肾损伤模型。实验设正常对照组,模型对照组和贝那普利治疗组。贝那普利4 mg/(kg.d)连续治疗8周后,测定24 h尿微量白蛋白及肾皮质丙二醛含量,检测超氧化物歧化酶活性,并通过PAS染色观察肾脏组织形态学变化。结果与模型对照组相比,贝那普利能显著降低24 h尿微量白蛋白及MDA含量,提高SOD活性(P<0.05)。PAS染色显示贝那普利能明显减少肾小管透明管型的形成。结论贝那普利对阿霉素致SD大鼠肾损伤具有一定的保护作用,其作用机制可能与其减少尿蛋白生成,并增强抗氧化酶活性,减少自由基对肾脏的氧化损伤有关。
Objective To observe the protective effect of benazepril on doxorubicin-induced renal injury in SD rats. Methods Adriamycin induced renal injury in SD rats. Experimental set up normal control group, model control group and benazepril treatment group. Benazepril 4 mg / (kg.d) for 8 consecutive weeks after treatment, determination of 24 h urinary albumin and renal cortical malondialdehyde content, detection of superoxide dismutase activity, and by PAS staining kidney histomorphology Variety. Results Compared with the model control group, benazepril significantly reduced 24 h urine microalbumin and MDA content, and increased SOD activity (P <0.05). PAS staining showed that benazepril significantly reduced tubular tubular formation. Conclusions Behenopril can protect renal injury induced by doxorubicin in SD rats. Its mechanism may be related to the decrease of urinary protein production, enhancement of antioxidant enzyme activity and reduction of oxidative damage of free radicals to the kidneys.