细胞色素2J3基因转染减轻大鼠胸主动脉球囊损伤后血管狭窄程度的初步机制  

The Initial Mechanism of CYP2J3 Transfection Lessen Rats' Artery Stenosis After Aortic Sac Injury

作　　者：常静[1] 芦玲巧[2] 曾翔俊[2] 王红霞[2] 张立克[2] 

机构地区：[1]首都医科大学附属北京佑安医院病理科,北京100069 [2]首都医科大学病理生理教研室,北京100069

出　　处：《微循环学杂志》2013年第4期24-26,I0001,共4页Chinese Journal of Microcirculation

摘　　要：目的:探讨细胞色素2J3(CYP2J3)基因转染减轻动脉球囊损伤后血管狭窄程度的初步机制。方法:36只实验大鼠,其中18只用于建立胸主动脉球囊损伤模型,余18只进行假手术。前者分为三组(n均=6),分别从尾静脉注入生理盐水,为动脉损伤模型组(I组)、CYP2J3(2J3I组)、pcDNA3.1(3.1I组);后者亦分为三组(n均=6),亦从尾静脉注入与上相同试剂,分别为假手术组(Sh组)、2J3Sh组和3.1Sh组。术后28天取各组大鼠胸主动脉,观察动脉环相对管腔面积(RLA)变化,检测细胞外信号调节激酶(ERK1/2)、内皮型一氧化氮合成酶(eNOS)蛋白表达。结果:动脉损伤各组大鼠RLA均小于相应Sh组(P<0.05或P<0.01);2J3I组RLA大于I组及3.1I组(P<0.01)。动脉损伤各组较相应Sh组磷酸化ERK1/2蛋白表达升高(P<0.05或P<0.01),2J3I组ERK1/2蛋白表达高于I组和3.1I组(P均<0.01)。动脉损伤各组eNOS蛋白表达低于相应Sh组(P<0.01);2J3I组eNOS蛋白表达高于I组和3.1I组(P均<0.01)。结论:CYP2J3基因转染可减轻动脉损伤后狭窄,其作用与其增加ERK1/2及eNOS蛋白表达有关。Objective:To investigate the initial mechanism of CYP2J3gene transfection lessen vascular stenosis after aortic sac injury.Method:Rats were divided into six groups randomly:I,Sh,2J3I,2J3Sh,3.1Iand 3.1Sh groups.28days after artery sac injury,the RLA,ERK1/2and eNOS protein levels in thoracic aorta were detected.Results:The data showed that the RLA of 2J3Igroup was higher than I group and 3.1I group(P<0.01).About ERK1/2protein content,2J3Igroup was higher than 3.1Igroup(P<0.01);however,the eNOS protein content of 2J3Igroup was higher than I group and 3.1Igroup(P<0.01).Conclusion:Up-regulating CYP2J3/EETs system can decrease the degree of artery stenosis after injury,which is relevant with increasing ERK1/2and eNOS protein levels.

关 键 词：胸主动脉球囊损伤 血管狭窄程度 基因转染 细胞色素 血管介入治疗 血管内皮细胞损伤 血管阻塞性疾病 术后血管再狭窄 

分 类 号：R543.1[医药卫生—心血管疾病]