ERK在17β-雌二醇抑制大鼠血管损伤后平滑肌细胞增殖中的作用

本实验旨在研究细胞外信号调节激酶(extmcellular signal-regulated kinase，ERK)在17β-雌二醇(17β-estra-diol，E2)介导的一氧化氮(nitric oxide，NO)抑制血管损伤后平滑肌细胞(vascular smooth musclecell，VSMC)增殖中的作用。在去势雌性大鼠中建立颈总动脉球囊损伤模型，实验分单纯去势组(OVX)、去势给予E2治疗组(E2 OVX)、去势后球囊损伤组(OVA Inj)和去势后球囊损伤给予E2治疗组(E2 OVA Inj)。分别检测各组血管壁的厚度、血浆中NO的浓度、ERK蛋白表达和活性的变化以及eNOS蛋白表达情况。结果显示，与OVX组相比，OVA Inj组血浆NO含量明显下降和血管壁厚度明显增厚，E2可增加血浆中NO含量和抑制球囊损伤后血管壁的增厚；E2可以抑制ERK蛋白表达和活化，诱导eNOS蛋白的表达。血浆中：NO含量与eNOS蛋白的表达呈正相关，与血管壁厚度和ERK蛋白表达呈负相关。以上结果提示，E2可通过增加血管组织eNOS蛋白表达，促进NO生成，抑制ERK蛋白的表达和活性，从而抑制血管损伤后VSMC的增殖。

Effect of ERK on 17beta-estradiol-induced inhibition of VSMC proliferation in rats after vascular injury

The aim of the present study was to investigate the effect of ERK on 17beta-estradiol (E(2)) inhibition of vascular smooth muscle cell (VSMC) proliferation in rats after vascular injury. Common carotid artery balloon-injury (Inj) model was established in ovariectomized rats (OVX). Female SD rats were randomly divided into 4 groups: OVX, E(2)+OVX, OVX+Inj, and E(2)+OVX+Inj groups. The thickness of the vessels, the plasma content of NO, and the expression of ERK, phosphorylated ERK as well as eNOS protein were measured. The results showed that compared with OVX, the vessel wall was significantly thickened and the plasma content of NO was significantly decreased in OVX+Inj group. E(2) significantly decreased the vessel thickness but increased the plasma NO content after balloon injury. E(2) inhibited the expression of ERK, phosphorylated ERK and induced the eNOS expression. There is a positive correlation between plasma NO content and eNOS protein expression, while there is a negative correlation between plasma NO content and the thickness of vessel. The plasma NO content and the expression of ERK protein were negatively correlated. These results suggest that E(2) increases the vascular eNOS protein expression and NO release, leading to the inhibition of VSMC proliferation after balloon injury by inhibiting the ERK and phosphorylated ERK protein expression.