体外培养中川芎嗪对大鼠血管平滑肌细胞血管细胞粘附分子-1表达的影响

Effects of Tetramethylpyrazine on Expression of Vascular Cell AdhesionMolecule-1 in Vascular Smooth Muscle Cells in Sprague Dawley Rat

目的 观察川芎嗪对血管平滑肌细胞 (VSMC)表达血管细胞粘附分子 1(VCAM 1)的影响。方法 在建立血管紧张素Ⅱ (AngⅡ )诱导的VSMC表达粘附分子模型的基础上 ,将培养的细胞分为 3组 :正常对照组、AngⅡ刺激组、川芎嗪治疗组。分别在 6、 12、 2 4h 3个时段 ,利用免疫细胞化学技术和原位杂交技术检测各组细胞中VCAM 1的蛋白表达及mRNA转录水平。结果 ①各时段正常对照组即有VCAM 1的基础表达 ;②与正常对照组比较 ,AngⅡ能够明显诱导VCAM 1的表达 ,而且其诱导作用在 6h即已出现 (P <0 0 5 ) ,12h表达增强 (P <0 0 1) ,2 4h有所回降 (P <0 0 5 ) ;③川芎嗪在各个时段均能抑制VCAM 1蛋白和mRNA的转录水平 (P <0 0 5 )。结论 AngⅡ能够明显诱导VSMC中VCAM 1的表达 ,而川芎嗪能够通过抑制VSMC中VCAM

Objective To evaluate the effects of tetramethylpyrazine (TMP) on the expression of vascular cell adhesion molecule 1 (VCAM 1) in cultured vascular smooth muscle cells (VSMC). Methods The model of an increased expression of VCAM 1 in Sprague Dawley rat aorta thoracalis VSMC induced by Angiotensin Ⅱ (AngⅡ) was developed. The cultured VSMC were divided into three groups: control group, AngⅡ goup, TMP group. The expression of VCAM 1 in each group was detected by different methods below at 6 h, 12 h, 24 h respectively: immunocytochemistry for the expression levels of VCAM 1 protein and in situ hybridization technique for those of VCAM 1 mRNA in VSMC.Results There was the basic expression of VCAM 1 in control group. The expression of VCAM 1 induced by AngⅡ was significantly increased as compared with control group. AngⅡ induced VCAM 1 accumulation appeared at 6 h ( P < 0 05), peaked at 12 h ( P <0 01), decreased at 24 h ( P <0 05). Compared with AngⅡ goup, the increased expression of VCAM 1 induced by AngⅡ could be inhibited by TMP significantly ( P <0 05) in different time points. Conclusion AngⅡ could significantly induce the expression of VCAM 1 in VSMC. The increased expression of VCAM 1 induced by AngⅡ could be inhibited by tetramethylpyrazine significantly, which may ameliorat the severity of the early AS lesion.