摘要
目的探讨磷脂酰肌醇-3-激酶(PI3K)/Akt信号转导途径在小鼠肾缺血再灌注损伤中作用及其机制。方法BALB/C小鼠随机分为3组。假手术组,共6只;对照组:采用双肾蒂阻断,缺血时间为35 m in,再灌注30 m in、90 m in、24 h、48 h,每时点6只小鼠;W ortm ann in药物组:缺血前4 h腹腔注射W ortm ann in,其余同对照组。观察缺血后肾功能和肾脏组织学改变,采用免疫组化技术检测p27和PCNA蛋白的表达。结果PI3K抑制剂W ortm ann in可加重小鼠肾缺血再灌注损伤后血肌酐和尿素氮的水平升高,加重肾小管的损伤程度;小鼠肾缺血再灌注损伤后细胞周期抑制蛋白p27水平降低,增殖细胞核抗原PCNA表达增加;W ortm ann in可抑制p27水平和肾小管细胞增殖。结论W ortm ann in可加重小鼠肾缺血再灌注损伤后肾功能和肾组织的损伤,抑制肾小管细胞增殖,提示PI3K/Akt信号通路在肾脏缺血再灌注损伤中起非常重要的调控作用。
Objective To investigated the role of PI3K/Akt pathway involved in renal ischemia/reperfusion injury in mice.Methods There were a total of 3 experimental groups.The sham-operative group was with 6 mice.The control and wortmannin-treated groups subjected to renal injury were similarly studied at 30min,90min,24h,48h(n=6) following reperfusion.Wortmannin or its vehicle was given intraperitoneally at 4 hours before mice were subjected to surgery.The clamping duration was thirty-five minutes.At above time points after reperfusion,serum creatinine,BUN and renal pathological changes were tested and compared among the three groups.Expressions of p27 and PCNA proteins were examined by immunohistochemistry.Results Wortmannin had a deleterious effect on serum creatinine and BUN values,renal impairments after renal ischemia-reperfusion injury of mice.The renal cell proliferation increased after ischemia/reperfusion injury in mouse,which could be inhibited by wortmannin.Renal p27 level significantly decreased in the wortmannin-treated group.Conclusions The study suggests that PI3-kinase/Akt signal pathway play an important role in regulating the repair following renal ischemia/reperfusion injury.
出处
《杭州师范学院学报（医学版）》
2006年第2期63-65,共3页
Journal of Hangzhou Teachers College :Medical Edition
