CAJ | 학술논문

目的：探讨细胞外信号调节激酶1/2（ ERK1/2）在高血压大鼠模型动脉外膜血管重塑中的作用。方法：利用血管紧张素II （ Ang II）微泵灌注制备高血压大鼠模型，随机分为未处理组、生理盐水灌注组和Ang II灌注组。分别检测各组大鼠尾动脉收缩压及血管形态学改变；Western blotting技术检测外膜成纤维细胞过氧化氢酶（ CAT）蛋白在未处理组、单纯Ang II、ERK1/2抑制剂PD98059和Ang II＋PD98059培养下的表达。结果：大鼠颈动脉HE染色和收缩压结果显示，与未处理组及生理盐水灌注组相比，Ang II组大鼠颈动脉中膜厚度和收缩压明显增加（P＜0.01），动脉形态结构有明显改变，并且有显著的病理性血管重塑发生。 Western blotting 检测结果显示， PD98059作用下CAT比单纯Ang II明显增高（P＜0.05），表明ERK1/2信号通路能够恢复Ang II诱导的CAT表达下调。结论：Ang II可能通过ERK1/2信号通路下调血管外膜CAT的表达，进而促进血管细胞表型转化，导致血管病理性重塑发生。
목적：탐토세포외신호조절격매1/2（ ERK1/2）재고혈압대서모형동맥외막혈관중소중적작용。방법：이용혈관긴장소II （ Ang II）미빙관주제비고혈압대서모형，수궤분위미처리조、생리염수관주조화Ang II관주조。분별검측각조대서미동맥수축압급혈관형태학개변；Western blotting기술검측외막성섬유세포과양화경매（ CAT）단백재미처리조、단순Ang II、ERK1/2억제제PD98059화Ang II＋PD98059배양하적표체。결과：대서경동맥HE염색화수축압결과현시，여미처리조급생리염수관주조상비，Ang II조대서경동맥중막후도화수축압명현증가（P＜0.01），동맥형태결구유명현개변，병차유현저적병이성혈관중소발생。 Western blotting 검측결과현시， PD98059작용하CAT비단순Ang II명현증고（P＜0.05），표명ERK1/2신호통로능구회복Ang II유도적CAT표체하조。결론：Ang II가능통과ERK1/2신호통로하조혈관외막CAT적표체，진이촉진혈관세포표형전화，도치혈관병이성중소발생。
AIM:To explore the effect of extracellular signal-regulated kinase 1/2 ( ERK1/2) on the vascular adventitial remodeling in a hypertension rat model .METHODS:The rats were randomly divided into control group , mini-pump infusion of saline group and mini-pump infusion of angiotensin II ( Ang II) group as the hypertension model .The sys-tolic pressure and vascular morphology of the rats were examined .Adventitial fibroblasts were treated with Ang II , PD98059 ( ERK1/2 inhibitor) and Ang II+PD98059.The catalase ( CAT) expression in the cells was detected by Western blotting . RESULTS:Compared with control group and mini-pump infusion of saline group , the systolic pressure and carotid media thickness (stained by HE) in mini-pump infusion of Ang II group were significantly increased (P<0.01).Meanwhile, ar-tery morphology in mini-pump infusion of Ang II group had obviously changed with a significant occurrence of pathological vascular remodeling .The result of Western blotting showed that the expression of CAT in the adventitial fibroblasts treated with Ang II+PD98059 was much higher than that in the cells treated with Ang II alone (P<0.05), indicating that down-regulation of CAT induced by Ang II was restored by ERK 1/2 signaling pathway .CONCLUSION:Ang II down-regulates CAT through ERK1/2 pathway and promotes cell phenotype transformation , which lead to pathological vascular remodeling .