摘要
目的 检测体外培养的系膜增生性肾小球肾炎 (MSPGN)肾小球系膜细胞的 JNK/ SAPK活性 ,并探讨其对细胞间粘附分子 1(ICAM- 1)的调控作用。方法 选取 6例正常人和 7例 MSPGN患者的肾组织 ,分别采用免疫沉淀和免疫印迹法检测体外培养的肾小球系膜细胞的 JNK/ SAPK活性 ,RT- PCR检测 ICAM- 1m RNA表达 ,流式细胞仪检测细胞表面 ICAM- 1平均荧光强度。结果 在自发培养条件下 ,与正常对照组相比 ,MSPGN组肾小球系膜细胞的 JNK/ SAPK明显增高 (P<0 .0 5 )。在 TNFα诱导下 ,两组肾小球系膜细胞的 JNK/ SAPK活性均有增加 ,但 MSPGN组仍高于正常对照组 (P<0 .0 5 )。经 TNFα诱导后 ,随着 JNK/ SAPK活性增强 ,ICAM- 1m RNA及其平均荧光强度也均增加 (P<0 .0 5 )。经蛋白激酶抑制剂 DMAP阻断后 ,随着 JNK/ SAPK活性下降 ,ICAM- 1m RNA及其平均荧光强度亦下降 (P<0 .0 1)。 MSPGN的 JNK/ SAPK活性与 ICAM- 1m RNA表达和ICAM- 1平均荧光强度呈正相关关系 (r=0 .6 94,P<0 .0 1)。结论 MSPGN的肾小球系膜细胞的 JNK/ SAPK存在异常活化 ,这种异常活化可能介导了 ICAM- 1的过度表达。
Objective To observe the activity of c Jun N terminal kinase/stress activated protein kinase(JNK/SAPK) and assess the correlation between JNK/SAPK activity and ICAM 1 expression on mesangial cells in mesangial proliferative glomerulonephritis(MSPGN). Methods Seven patients with MSPGN and 6 controls were selected for this study.JNK/SAPK activity was detected by immunoprecipitation and western blotting; RT PCR was used to detect ICAM 1 mRNA expression, and flow cytometry was used to analyze cell surface ICAM 1 expression. Results Either in spontaneous condition or under the stimulus of TNFα, the activity of JNK/SAPK on mesangial cells in vitro in MSPGN was higher than that of the controls ( P <0.05); the activity of JNK/SAPK in MSPGN was found to have a positive correlation with the levels of ICAM 1 mRNA and protein. The levels of ICAM 1 mRNA and protein were increased by TNFα stimulation while the levels ICAM 1 mRNA and protein were decreased by DMAP inhibition ( P <0.01). Conclusion JNK/SAPK may have been aberrantly activated in MSPGN, which may involve in the overexpression of ICAM 1 in MSPGN.
出处
《华西医科大学学报》
CAS
CSCD
北大核心
2001年第2期277-280,共4页
Journal of West China University of Medical Sciences
