兔髂动脉再狭窄模型中连接蛋白的表达  

The expression of connexin in rabbit iliac artery restenosis models

作　　者：曹路[1] 赵翠[2] 丛洪良[1] 毛用敏[3] 赵莉莉[3] 王霁翔[1] 王菁[4] 赵福梅[3] 

机构地区：[1]天津市胸科医院心内科,天津300222 [2]中国人民武装警察部队后勤学院附属医院心内科 [3]天津市心血管病研究所 [4]天津市胸科医院病理科

出　　处：《临床心血管病杂志》2014年第12期1115-1120,共6页Journal of Clinical Cardiology

基　　金：天津市卫生局科技基金(No:11KG123;2013KR18)

摘　　要：目的:通过建立兔髂动脉再狭窄模型,观察髂动脉病理改变及连接蛋白(Cx)的表达情况。方法:20只新西兰大白兔随机分为对照组与再狭窄组,采用高脂饲料喂养联合兔髂动脉二次球囊损伤建立再狭窄模型。所有髂动脉标本均行HE染色及免疫组织化学检测,采用RT-PCR法测定血管组织匀浆Cx43及Cx40mRNA表达。结果:与对照组相比,再狭窄组髂动脉管腔狭窄率增大[(23.00±3.53)%︰(89.32±6.93)%,P<0.01],内膜明显增厚[(266.12±70.27)μm︰(2.85±0.19)μm,P<0.01],α-平滑肌肌动蛋白(α-SMA)染色证实新生内膜主要细胞成分为血管平滑肌细胞(VSMCs)。免疫组织化学结果显示,两组均有Cx43表达,再狭窄组新生内膜处有大量Cx43表达,较正常对照组明显增强。两组血管ECs及中膜均有Cx40表达,再狭窄组Cx40表达仅比对照组略有增强。RT-PCR结果显示,与正常对照组比较,再狭窄组Cx43mRNA表达增加(P<0.01);但两组Cx40mRNA表达量差异无统计学意义。结论:新生内膜增殖是再狭窄的病理基础,VSMCs是主要的增殖细胞成分,并且这一过程伴随有Cx43的表达增加,而Cx40表达无变化。Objective.. To observe the pathological changes and expression of connexin（Cx） in rabbit iliac artery restenosis models. Method.. Twenty New Zealand White rabbits were randomly divedied into 2 groups., control group（n= 10） and restenosis group（n= 10）. Restenosis group followed high-fat diet combined with d0uble-balloon injury to establish restenosis model. Four weeks later, all rabbits were killed and iliac arteries were then cut down for HE staining, immunohistochemiscal analysis, and detecting the expression of Cx mRNA by RT-PCR as well. Result^Computer-assisted histomorphometric analysis showed the intima thickness o restenosis group increased compared with that of control group [（266.12±70.27）μm vs（2.85±0.19）μm, P〈0.01]. We also observed the stenosis rates of restenosis group were higher than those of controls [-（89.32±6.93）% vs （23.00±3.53）%, P〈 0.01]. By using immunohistochemistry to detect a-smooth muscle actin （α-SMA）, we confirmed that the prolifer- ated cells in neointima were VSMCs in restenosis group. Immuohistochemical analysis indicated Cx43 expressed in all iliac arteries of two groups. Compared with controls, more Cx43 expression was detected in neointima in rest- enosis group. Additionally, the Cx40 expression of controls was a little lower than that of restenosis group. Com- pared with control group, the expression of Cx43 mRNA increased in restenosis group （P〈0.01）. As for the ex- pression of Cx40 mRNA, there was no difference between two groups. Conclusion： It is not Cx40 but Cx43 in gap junction that contributes to the process of the migration and proliferation of VSMCs in neointima formation, which plays an important role in the pathogenesis of restenosis.

关 键 词：再狭窄 血管平滑肌细胞 新生内膜增殖 连接蛋白43 连接蛋白40 

分 类 号：R543.1[医药卫生—心血管疾病]