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目的探讨一氧化氮(nitric oxide,NO)对单侧输尿管梗阻(unilateral ureteral obstruction,UUO)大鼠肾脏间质纤维化的作用及其可能的非血流动力学作用机制。方法成熟Sprague-Dawley雄性大鼠24只,随机分为4组:Ⅰ组假手术组、Ⅱ组模型组、Ⅲ组L-精氨酸(L-Arginine)组、Ⅳ组L-NG-硝基精氨酸甲酯(L-NAME)组。UUO术后28d处死各组大鼠,应用病理染色技术检测肾组织小管间质损伤指数,免疫组织化学法检测肾组织纤维连接蛋白(fibronectin,FN),RT-PCR技术检测肾组织精氨酸酶(Ar-ginase)mRNA的表达。结果与Ⅰ组相比,Ⅱ组肾脏小管间质损伤指数及肾脏组织FN的表达增加(P<0.01);与Ⅱ组相比,Ⅲ组损伤指数及FN的表达减少(P<0.01),Ⅳ组增加(P<0.01)。与Ⅰ组相比,Ⅱ组肾组织Arginase mRNA表达升高(P<0.01);与Ⅱ组相比,Ⅲ组Arginase mRNA表达降低(P<0.05),Ⅳ组升高(P<0.01)。结论NO通过减少细胞外基质(extracellular matrix,ECM)增生延缓肾脏间质纤维化,其对肾脏的保护机制可能部分是通过降低肾脏组织中Arignase mRNA的表达而实现的。
Objective To investigate the effect of nitric oxide (NO) on renal interstitial fibrosis in unilateral ureteral obstruction (UUO) rats and its possible non-hemodynamic mechanism. Methods Twenty-four male Sprague-Dawley rats were randomly divided into 4 groups: sham-operation group I, model group II, group L-arginine, group L-NG-nitro Arginine methyl ester (L-NAME) group. Rats in each group were sacrificed 28 days after UUO. The tubulointerstitial injury index of renal tissues was detected by pathological staining. Fibronectin (FN) was detected by immunohistochemistry and arginase (Ar-ginase) mRNA expression. Results Compared with group Ⅰ, the tubulointerstitial injury index and the expression of FN in renal tissue were increased in group Ⅱ (P <0.01); Compared with group Ⅱ, the injury index and the expression of FN in group Ⅲ were decreased (P <0.01); Ⅳ Group increased (P <0.01). Compared with group Ⅰ, the expression of Arginase mRNA in group Ⅱ increased (P <0.01). Compared with group Ⅱ, the expression of Arginase mRNA in group Ⅲ decreased (P <0.05), and increased in group Ⅳ (P <0.01). Conclusion Nitric oxide can delay renal interstitial fibrosis by reducing the proliferation of extracellular matrix (ECM), and its protective mechanism on the kidney may be partly through reducing Arignase mRNA expression in the kidney.