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目的 探讨c Jun氨基末端激酶 激活蛋白 1信号通路在肾小球肾炎单核细胞趋化蛋白1表达中的作用。方法 实验性肾炎应用兔抗鼠肾小球基底膜肾毒血清制备。应用凝胶电泳迁移率、超迁移实验和非放射性激酶活性检测法检测实验性肾炎肾组织和体外培养的肾小球系膜细胞内激活蛋白 1活化及其组成以及c Jun氨基末端激酶活性 ,应用核酸酶保护法检测体外培养的肾小球系膜细胞中单核细胞趋化蛋白 1表达。结果 实验性肾炎大鼠肾组织中c Jun氨基末端激酶和激活蛋白 1活性明显增强 ,分别是正常对照组的 (3 82± 0 5 8)倍和 (5 36± 0 6 1)倍 ,活化的激活蛋白 1主要含有c Jun和c Fos亚基 ;c Jun氨基末端激酶和激活蛋白 1活化与单核细胞趋化蛋白 1表达呈显著正相关。血管紧张素Ⅱ可诱导体外培养的肾小球系膜细胞单核细胞趋化蛋白 1表达、c Jun氨基末端激酶和激活蛋白 1活化 ,其作用呈剂量依赖性增加 ,10 0nmol/L血管紧张素Ⅱ诱导单核细胞趋化蛋白 1表达、c Jun氨基末端激酶和激活蛋白 1活性增加分别是对照组的 (2 0 99± 4 71)倍、(6 91±1 6 5 )倍和 (7 82± 1 32 )倍 ;应用c Jun氨基末端激酶特异性抑制剂SP6 0 0 12 5显著抑制血管紧张素Ⅱ诱导激活蛋白 1活化和单核细胞趋化蛋白 1表达。结论 血管紧张素Ⅱ可通?
Objective To investigate the role of c-Jun N-terminal kinase-1 signal pathway in the expression of monocyte chemoattractant protein-1 in glomerulonephritis. Methods Experimental nephritis rabbit anti-rat glomerular basement membrane nephrotoxic serum preparation. Application of electrophoretic mobility shift assay, ultra-migration assay and non-radioactive kinase activity assay were used to detect activation of activin-1 and its components and c-Jun N-terminal kinase activity in experimental glomerular mesangial cells and cultured renal glomerular mesangial cells The nuclease protection assay was used to detect the expression of monocyte chemotactic protein 1 in mesangial cells cultured in vitro. Results The activities of c-Jun N-terminal kinase and activin-1 in renal tissue of experimental nephritis rats were significantly increased, which were respectively (3 82 ± 0 58) and (5 36 ± 0 6 1) times higher than that of the normal control group Activator 1 mainly contains c Jun and c Fos subunits; c Jun N-terminal kinase and activator protein 1 activation and monocyte chemotactic protein 1 expression was positively correlated. Angiotensin Ⅱ induced the expression of monocyte chemoattractant protein-1 in glomerular mesangial cells cultured in vitro and the activation of c-Jun N-terminal kinase and activator protein 1 in a dose-dependent manner. The effect of angiotensin on 100 nmol / L Ⅱ induced monocyte chemoattractant protein-1 expression. The increase in c-Jun N-terminal kinase and activin-1 activity were (2 0 99 ± 4 71) times, (6 91 ± 1 6 5) times and ± 1 32) fold; the application of c-Jun N-terminal kinase-specific inhibitor SP6 0 0 12 5 significantly inhibited angiotensin Ⅱ-induced activation of activin-1 and monocyte chemotactic protein-1 expression. Conclusion Angiotensin Ⅱ can pass?