论文部分内容阅读
目的探讨人工合成E-选择素对大鼠局部脑缺血再灌注损伤脑组织中血管细胞黏附分子-1(VCAM-1)及其mRNA表达的影响。方法采用改良的Zea Longa法建立脑缺血再灌注损伤模型,60只雄性SD大鼠随机分为模型组、假手术组和治疗组。采用免疫组化法观察缺血区脑组织中微血管VCAM-1阳性细胞数,RT-PCR法观察其mRNA表达。结果①模型组VCAM-1阳性细胞在再灌注2 h后开始出现,并持续增多,24 h后达高峰,72 h开始下降,各时间点比假手术组明显增多(P<0.01);VCAM-1 mRNA在再灌注2 h后开始表达,12 h后达高峰,24 h开始降低,各时间点比假手术组明显增高(P<0.01)。②假手术组VCAM-1阳性细胞数少见,VCAM-1 mRNA表达水平低。③治疗组(24 h)VCAM-1阳性细胞数比假手术组增多(P<0.05),但较模型组少(P<0.05);VCAM-1 mRNA表达比假手术组高(P<0.05),但较模型组低(P<0.05)。结论大鼠局灶性脑缺血再灌注损伤后,VCAM-1及VCAM-1 mRNA表达增多;人工合成E-选择素可降低VCAM-1及VCAM-1 mRNA的表达从而抑制白细胞与血管内皮细胞黏附,减轻炎症反应和脑缺血再灌注损伤,发挥脑保护作用。
Objective To investigate the effect of synthetic E-selectin on the expression of vascular cell adhesion molecule-1 (VCAM-1) and its mRNA in the brain tissue of rats with focal cerebral ischemia-reperfusion injury. Methods The model of cerebral ischemia-reperfusion injury was established by the modified Zea Longa method. Sixty male SD rats were randomly divided into model group, sham-operation group and treatment group. Immunohistochemistry was used to observe the number of VCAM-1 positive cells in the ischemic brain tissue and the mRNA expression was observed by RT-PCR. Results ① VCAM-1 positive cells in model group began to appear 2 h after reperfusion, and continued to increase, peaked at 24 h, then decreased at 72 h, and significantly increased at each time point compared with sham operation group (P <0.01); VCAM- 1 mRNA began to express at 2 h after reperfusion, reached the peak at 12 h, then decreased at 24 h, and significantly increased at all time points (P <0.01). ② The number of VCAM-1 positive cells in sham operation group was rare, and the expression level of VCAM-1 mRNA was low. ③The number of VCAM-1 positive cells in the treatment group (24 h) increased more than that in the sham operation group (P <0.05), but less in the model group (P <0.05) , But lower than the model group (P <0.05). Conclusions The expression of VCAM-1 and VCAM-1 mRNA increases after focal cerebral ischemia-reperfusion injury in rats. Synthesized E-selectin can decrease the expression of VCAM-1 and VCAM-1 mRNA and inhibit the expression of VCAM-1 and VCAM- Adhesion, reduce inflammation and cerebral ischemia-reperfusion injury, play a role in brain protection.