儿茶素对肾病大鼠血浆及肾皮质内皮素、一氧化氮表达影响的研究

Effects of catechin on expressions of ET and NO in rats with nephrotic syndrome

目的 观察儿茶素对阿霉素肾病鼠血浆及肾皮质内皮素 (ET)、一氧化氮 (NO)表达的影响。方法 将 36只SD雌性大鼠随机分成正常组、肾病组、激素组、儿茶素预防组、儿茶素治疗组、儿茶素 +激素联合治疗组共 6组。应用生化法测定 2 4h各组尿蛋白排泄量、尿、血浆及肾局部中NO的浓度 ;应用放免法测定血浆及肾局部中ET的浓度 ;应用免疫组化法测定肾组织中固有细胞细胞增生核抗原 (PCNA)的表达 ;并应用半定量评分法对各组大鼠病理改变进行计量分析。结果 (1)实验末 ,大鼠血浆及肾皮质中NO浓度以肾病组为最低 (13 5± 3 7,2 7 8± 12 4 ) ,其他从低到高依次是儿茶素治疗组 (2 5 3± 5 3,4 2 5± 1 9)、儿茶素预防组 (36 8± 5 3,5 5 5± 15 4 )、激素组 (43 3± 4 0 ,73 6±15 8)、儿茶素 +激素联合治疗组 (5 4 3± 7 1,96 4± 17 2 ) (F =6 2 3,79 4 ,P <0 0 1) ;血浆及肾皮质中ET浓度则以肾病组最高 (5 72± 91,14 93± 2 99) ,其他组从高到低顺序与NO浓度从低到高的顺序相同(F =5 4 8,14 6 8,P <0 0 1) ,以儿茶素 +激素联合治疗组为最低 ;各组与肾病组相比 ,差异均有显著意义。 (2 )各组肾小球系膜细胞、上皮细胞、内皮细胞 ,肾小管上皮细胞 。

Objective Endothelin (ET) and nitric oxide (NO) play an important role in the occurrence and progression of renal diseases Recently their direct effects on the glomerulus have been observed Catechin is extracted from the green tea and is the main component of tea polyphenoles Catechin is a significant non enzyme anti oxidizer The anti oxidization of catechin is 20 times higher than that of vitamin E, and 6 times higher than that of superoxide dismutase (SOD) In addition, catechin shows the ability of anti agglutination and accelerating fibrinolysis In order to elucidate the partial possible mechanism of catechin on the treatment of nephrotic syndrome and the prevention of chronic renal injuries, the effect of catechin on expressions of NO and ET in plasma and renal cortex was investigated Methods Thirty six female SD rats were randomly divided into six groups, control, nephrotic, and dexamethasone treated, catechin prevented, catechin treated, and dexamethasone plus catechin treated groups At the end of the experiment, the excretion of 24 hrs urinary protein and the concentrations of the plasma and renal cortex NO were detected by means of the biochemistry assay The concentrations of the plasma and renal cortex ET were detected by means of the radioimmunoassay (RIA) The expression of PCNA in renal intrinsic cells was measured with the immunohistochemical technique A semiquantitative score was used to evaluate the injury degree of the glomeruli and tubulointerstitium Results At the end of the experiment, the concentrations of the plasma and renal cortex NO were (13 5±3 7) and (27 8±12 4) in the nephrotic group,(25 3±5 3) and (42 5±1 9)in the catechin treated group (36 8±5 3) and (55 5±15 4,) in the catechin prevented group,(43 3±4 0) and (73 6±15 8)in the dexamethasone treated group and, (54 3±7 1) and (96 4±17 2)in the dexamethasone plus catechin treated group ( F =62 3,79 4, P <0 01) While the concentrations of the plasma and renal cortex ET were (572±91) and (1 493±29) in the nephrotic group, which was the highest, (417±54) and (1 220±126) in the catechin treated, (398±76) and (1 023±134) in the catechin prevented, (300±88) and (951±235) in the dexamethasone treated and, (237±66) and (774±127) in the dexamethasone plus catechin treated groups (except P <0 05 in the catechin treated group, all others P <0 01) PCNA expressions of glomerular mesangial cells, visceral glomerular epithelial cells, glomerular endothelial cells, tublule epithelial cells and vascular endothelial cells were higher in the nephrotic group than those in the other groups (compared with the nephrotic group, P <0 05 in the catechin treated group, P <0 01 in all other groups) Compared with the nephrotic group, the renal pathologic scores were significantly different among the nephrotic group, catechin treated group (6 80±0 84, P <0 05), catechin prevented group (6 50±1 00, P <0 01), dexamethasone treated group (4 40±0 89, P <0 01), and dexamethasone plus catechin treated group (3 40±0 55 , P <0 01) The renal pathologic scores were positively correlated with the expression of PCNA, the concentrations of the plasma and renal cortex ET, the excretion of 24 hrs urinary protein ( P <0 01), and were negatively correlated with the concentrations of the plasma and renal cortex NO ( P <0 01) Conclusion Catechin slowed the chronic progressive renal lesions, which might be achieved by the increase of the renal cortex and plasma NO concentrations, the decrease of the renal cortex and plasma ET concentrations, the inhibition of the renal intrinsic cells proliferation, and the reduction of the 24 hrs urinary protein excretion