VEGF单克隆抗体对胰腺缺血再灌注损伤中细胞凋亡的影响  

Protective effect of VEGF McAb on pancreas ischemic/reperfusion of rats

作　　者：杨家红[1] 谢嵘[1] 王莹[2] 范昕[1] 

机构地区：[1]江苏大学附属医院普外科,江苏镇江212001 [2]江苏大学附属医院内分泌科,江苏镇江212001

出　　处：《江苏大学学报（医学版）》2009年第1期50-52,共3页Journal of Jiangsu University：Medicine Edition

摘　　要：目的:从胰腺腺泡细胞凋亡的角度探讨血管内皮生长因子(VEGF)单克隆抗体在胰腺缺血再灌注损伤中保护作用。方法:采用钳闭大鼠腹腔干、肠系膜上动脉制备胰腺缺血再灌注损伤模型,并应用细胞凋亡原位标记法(TUNEL)、免疫组化技术等检测VEGF单克隆抗体干预后对胰腺细胞凋亡及Bax,Bcl-2蛋白表达的影响。结果:干预组15,30,60 min胰腺细胞凋亡指数显著低于缺血再灌注组(P<0.01)。正常胰腺组织未见凋亡调控基因Bcl-2的表达,VEGF单克隆抗体干预后15,30,60 min胰腺细胞Bcl-2染色阳性率明显高于缺血再灌注组(P<0.01);正常胰腺组织见较弱的凋亡调控基因Bax的表达,而VEGF单克隆抗体干预后15,30,60 min胰腺细胞Bax染色阳性率明显低于缺血再灌注组(P<0.01)。结论:VEGF单克隆抗体能够通过抑制胰腺腺泡细胞的过度凋亡减轻胰腺炎的严重程度,该作用可能是通过促进抗凋亡Bcl-2基因表达,抑制促进凋亡基因Bax表达来实现的。Objective： To investigate the effect of VEGF McAb protecting on pancreas injury during experimental ischemic/reperfusion in rats.Methods： Ischemic/reperfusion models were made by ligated both the anterior menseneric artery and the celica artery of 70 rats.Apoptosis of pancreatic acinar cells was detected by terminal deoxynucleotidyl transferase mediated dUTPbiot in nick end labeling（TUNEL） method,and the expression of apoptosis regulated gene Bax and Bcl-2 was detected by immunohistochemical technique. Results： The index of apoptosis increased significantly in pancreatic tissues after pancreatic ischemia/reperfusion injury but offset by administration of VEGF McAb.Immunohistochemical analysis showed that just weak Bax staining cells were detected,with no Bcl-2 positive staining cells in normal pancreatic tissues.The positive rate of Bcl-2 protein in VEGF McAb group was significantly higher than ischemic/reperfusion group while the positive rate of Bax was significantly lower（all P〈0.01）. Conclusion： VEGF McAb treatment alleviated pancreatic ischemia/reperfusion injury by restraining excessive apoptosis.This effect might be related with up-regulating the expression of Bcl-2 and down-regulating the expression of Bax.

关 键 词：胰腺 缺血再灌注 细胞凋亡 VEGF单克隆抗体 BAX Bcl-2 

分 类 号：R576[医药卫生—消化系统]