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目的 :探讨一氧化氮 (NO)在阿霉素 (ADR)肾病病鼠发病中的作用及其机制。 方法 :复制阿霉素肾病模型 ,分别用L 精氨酸 (L Arg)及N 硝酸 L 精氨酸甲基酯 (L NAME)进行干预 ,用硝酸还原酶法测定肾皮质匀浆NO代谢产物NO-2 /NO-3 水平来反映NO水平 ,用末端标记法和免疫组化法分别检测皮质部细胞凋亡和Bcl 2、Bax、c Myc蛋白表达情况 ,用原位杂交法测定皮质部细胞p5 3 mRNA转录水平。 结果 : ①ADR组肾皮质匀浆NO-2 /NO-3 水平明显低于对照组 (P <0 0 1) ,皮质部细胞凋亡数、p5 3 mRNA水平和c Myc蛋白表达均分别明显高于对照组 (P均小于 0 0 1) ,肾小管细胞Bcl 2蛋白表达明显低于对照组而Bax蛋白表达却明显高于对照组 (P均小于0 0 1)。②ADR +L Arg组肾皮质匀浆NO-2 /NO-3 水平明显高于ADR组 (P <0 0 1) ,皮质部细胞凋亡数、p5 3 mRNA水平和c Myc蛋白表达则分别明显低于ADR组 (P均小于 0 0 5 ) ,肾小管细胞Bcl 2蛋白表达明显高于ADR组而Bax蛋白表达则明显低于ADR组 (P均小于 0 0 5 )。③ADR +L NAME组肾皮质匀浆NO-2 /NO-3 水平明显低于ADR组(P <0 0 1) ,皮质部细胞凋亡数、p5 3 mRNA水平和c Myc蛋白表达均明显高于ADR组 (P均小于 0 0 5 ) ,肾小管细胞Bcl 2蛋白表达明显低于ADR组而肾小管细胞Ba
Objective: To investigate the role of nitric oxide (NO) in the pathogenesis of adriamycin-induced nephropathy in rats and its mechanism. Methods: The model of adriamycin nephropathy was duplicated. L Arg and L NAME were respectively used for the intervention. Nitric acid reductase was used to determine NO metabolites NO -2 / NO-3 levels to reflect the level of NO. End-labeling and immunohistochemistry were used to detect the apoptosis of cortical cells and the expression of Bcl-2, Bax and c-Myc proteins, respectively. The in situ hybridization was used to detect the expression of p5 3 mRNA transcription level. Results: ① The level of NO-2 / NO-3 in renal cortex homogenate of ADR group was significantly lower than that of control group (P <0.01), and the number of cortical apoptosis, p5 3 mRNA and c Myc protein expression were significantly higher In the control group (P <0.01), the expression of Bcl-2 in tubular cells was significantly lower than that in the control group, while the expression of Bax protein in the control group was significantly higher than that in the control group (P <0.01). ② The level of NO-2 / NO-3 in renal cortex homogenate of ADR + L Arg group was significantly higher than that of ADR group (P <0.01), and the number of cortical cell apoptosis, p5 3 mRNA and c Myc protein expression were significantly lower In the ADR group (P <0.05), the expression of Bcl-2 in tubular cells was significantly higher than that in ADR group, while the expression of Bax protein was significantly lower than that in ADR group (P <0.05). ③ The level of NO-2 / NO-3 in renal cortical homogenate of ADR + L NAME group was significantly lower than that of ADR group (P <0.01), the number of cortical apoptosis, p5 3 mRNA and c Myc protein expression were significantly higher ADR group (P <0.05), the expression of Bcl-2 protein in renal tubular cells was significantly lower than that in ADR group and tubular cells Ba