摘要
目的应用JNK抑制剂SP600125研究转录因子c-Jun的激活对肾缺血/再灌注(I/R)诱导细胞凋亡的影响。方法采用双侧夹闭大鼠肾蒂缺血45 min后再灌注3 h的方法制备肾I/R动物模型。免疫组化法分析转录因子c-Jun的激活变化情况;原位末端标记法(TUNEL)检测肾小管上皮细胞凋亡情况。结果再灌注3h,p-c-Jun的免疫活性显著增强,凋亡的细胞数明显增加。SP600125明显抑制了p-c-Jun的免疫活性且明显减少肾I/R诱导的细胞凋亡。结论肾I/R诱导的细胞凋亡与c-Jun的激活有关,SP600125能明显抑制转录因子c-Jun的激活,减轻肾小管上皮细胞的凋亡。
Objective Using SP600125, a reversible ATP competitive inhibitor of JNK, to explore the effect of c - Jun activation mechanism induced by renal ischemia/reperfusion （I/R） on the apoptosis of renal tubular epithelial cells. Methods The model of bilateral post - ischemic renal injury was established in rats by clamping the renal pedicles for 45 minutes and allowing subsequent reperfusion for 3 h. p - c - Jun Immunohistochemical staining was used to investigate the effect of SP600125 on the activation of c - Jun. Terminal deoxynucleotidyl transferase mediated dUTPnick end labeling （TUNEL） method was used to assess the apoptosis of renal tubular epithelial cells. Results As indicated in the tables, the immunoreactivity of p - c - Jun and the number of apoptotic cells were significantly increased after I/R, as compared with that of the sham operation group. Administration of SP600125 60 min before renal ischemia could significantly inhibit the immunoreactivity of p - c - Jun and decrease the number of apoptotic cells. Conclusion The activation of c - Jun is related to the I/R - induced renal tubular epithelial cell apoptosis ; SP600125 can inhibit the renal tubular epithelial cell apoptosis by suppressing the activation of c - Jun.
出处
《徐州医学院学报》
CAS
2007年第9期578-581,共4页
Acta Academiae Medicinae Xuzhou
基金
江苏省高校自然科学研究计划项目(03KJB310144)
徐州医学院附属医院课题(2006-37
2007-21)
