摘要
目的探讨慢性肾功能不全大鼠肾组织磷酸化P42/p44丝裂原活化蛋白激酶(P-P42/p44 MAPK)的表达特征及其可能的作用。方法16只Wistar大鼠随机分成实验组和对照组,每组8只。采用5/6肾切除方法构建慢性肾功能不全大鼠模型,术后120d处死大鼠,取大鼠肾组织行石蜡切片,PAS染色观察大鼠肾脏病理改变,免疫组化和Western blot法分别检测大鼠肾组织磷酸化P42/p44丝裂原活化蛋白激酶的表达特征及活性变化。结果术后120d实验组大鼠与对照组相比,出现明显的肾小球硬化和肾小管坏死等慢性肾功能不全的典型病理特征,免疫组织化学染色检测磷酸化p42/p44 MAPK黄棕色染色颗粒明显增加。Western-blot结果显示,实验组大鼠肾组织磷酸化P42/p44丝裂原活化蛋白激酶(P-P42/p44 MAPK)活性表达水平明显上调(P<0.01)。结论磷酸化P42/p44丝裂原活化蛋白激酶在慢性肾功能不全大鼠模型的肾组织中活性明显升高,可能是慢性肾功能不全时各种细胞外刺激因素介导肾脏纤维化的重要途径之一。
Objective To study the expression and possible role of P-P42/p44 MAPK in the kidney of 5/6 nephrectomy rats. Methods 16 Wistar rats were randomly divided into control and experimental groups （n=8）. The remnant kidney model was constructed through 2-stage 5/6 nephrectomy. 8 control and 8 experimental rats were killed 4 months after the second operation. Remnant kidneys were isolated. Tissues were paraffin embedded, sliced and stained by PAS. The expression of P-P42/p44 MAPK was analysized via immunohistochemical stainning and Western blot. Results 120 days after operation, there were severe glomerular injury characterized by tubulointerstitial lesions, glomerulosclerosis and enhanced expression of P-P42/p44 MAPK in the kidney of 5/6 nephrectomy rats （P〈0.01）, compared with the control group. Conclusion Activated P42/p44 MAPK pathway may, in part, play a role in the pathogenesis of renal fibrosis of chronic renal failure.
出处
《中国组织化学与细胞化学杂志》
CAS
CSCD
2007年第2期215-218,共4页
Chinese Journal of Histochemistry and Cytochemistry
