银杏总黄酮对肾缺血再灌注大鼠p-JNK表达的影响  

Effect of total flavone of Gingko on phosphorylation of JNK in rats with renal ischemia reperfusion injury

作　　者：朱家军[1] 夏安周[2] 王妍妍[2] 张探[2] 李娜[2] 

机构地区：[1]江苏省灌云县人民医院,江苏灌云222200 [2]徐州医学院,江苏徐州221004

出　　处：《实用临床医药杂志》2011年第3期11-14,共4页Journal of Clinical Medicine in Practice

基　　金：江苏省连云港市科研基金资助项目(ZC243);徐州医学院横向科研合作课题

摘　　要：目的观察肾缺血再灌注损伤(IRI)后JNK活化的变化,并探讨银杏总黄酮(TFG)对其影响。方法 SD大鼠随机分为假手术组(Sham,n=12)、缺血再灌注组(IR,n=30)和银杏总黄酮处理组(TFG,n=12)。采用夹闭双侧肾动静脉45min然后松开动脉夹制备肾IRI模型。蛋白免疫印迹检测肾组织中p-JNK的表达,并用细胞凋亡原位末端标记(TUNEL法)检测肾小管上皮细胞凋亡。结果 IR组肾组织中p-JNK的表达在再灌注10 min开始升高,再灌注30 min达到高峰,再灌注1 h有所降低,再灌注24 h再次升高,同时该时段有大量肾小管上皮细胞凋亡;给予TFG处理,再灌注30 min p-JNK表达明显减弱,再灌注24 h细胞凋亡明显减少。结论 TFG防治肾IRI机制可能与抑制肾组织中JNK磷酸化的程度,减少肾小管上皮细胞凋亡有关。Objective To investigate the change of phosphorylation of JNK in renal ischemia reperfusion injury（IRI）and study the effect of total flavone of Gingko（TFG）on JNK activation.Methods Male Sprague Dawley rats were randomly divided into sham-operation group（Sham,n=12）,ischemia reperfusion groups（IR,n=30） and TFG groups（TFG,n=12）.The models were established through clamping bilateral renal arteries for 45 min and then reperfusion.Tubular cell apoptosis was confirmed by terminal deoxynucleotidyl transferase（TDT） mediated dUTP biotin nick end labeling（TUNEL） assay;The phosphorylation of JNK were detected by Western blotting analysis.Results In the IR group,the levels of tubular cell apoptosis significantly increased;activation of JNK was observed in the kidney as early as 10 mins after reperfusion,reaching its peak 30 min after and declined 1 h after,but increasd 24 h after reperfusion.Pretreatment with TFG decreased significantly the levels of tubular cell apoptosis;it also decreased the phosphorylation level of JNK compared with that in the IR group.Conclusion The results showed that the mechanism of TFG to protect the renal IRI may be associated with decreasing the phosphorylation of JNK,and therefore inhibiting apoptosis of tubular epithelial cells.

关 键 词：缺血再灌注 银杏总黄酮 C-JUN氨基末端激酶 肾 

分 类 号：R692[医药卫生—泌尿科学]