摘要
目的探讨七氟醚预处理对大鼠脑缺血再灌注损伤后含核转录因子κB(NF-κB)反应元件的蛋白细胞黏附分子[细胞间黏附分子-1(ICAM-1)和血管细胞黏附分子-1(VCAM-1)]、基质金属蛋白酶-2(MMP-2)和基质金属蛋白酶-9(MMP-9)的影响。方法雄性SD大鼠随机分为假手术组、缺血组和七氟醚预处理组。采用线栓法制备大脑中动脉栓塞大鼠模型。Western blot检测缺血再灌注6、24、48和72 h后缺血侧ICAM-1、VCAM-1、MMP-2和MMP-9表达。伊文思蓝(EB)染色观察血脑屏障的通透性。结果七氟醚预处理组缺血侧脑组织中EB含量显著低于缺血组(P<0.01)。缺血组各再灌注时间点ICAM-1、VCAM-1、MMP-2和MMP-9表达均显著高于七氟醚预处理组。结论七氟醚预处理可能通过抑制再灌注损伤后含NF-κB反应元件的ICAM-1、VCAM-1、MMP-2和MMP-9的上调起神经保护作用。
Aim To study the effect of sevoflurane preconditioning on proteins, including cellular adhesion molecules(CAMs) and matrix metalloproteinases(MMPs), with regulatory element κB after cerebral ischemia and reperfusion(I/R) in rats. Methods Transient focal cerebral I/R was induced by using 60 min of middle cerebral artery occlusion(MCAO) in adult male Sprague-Dawley rats. The animals were exposed for 30 min per day on 4 consecutive days to ambient air(sham and vehicle group) or to 1.2% sevoflurane(sevo-pre group), and then subjected to MCAO 24 hours later. Blood-brain barriers(BBB) integrity was detected by Evans blue extravasation at 48 hours after ischemia. Biochemical measurements for intracellular adhesion molecule-1(ICAM-1), vascular cell adhesion molecule-1(VCAM-1), MMP-2 and MMP-9 were conducted at 6 to 72 hours after I/R. Results Evans blue extravasation showed that the total EB content was lower in sevopre group than in vehicle group(P<0.01). Ischemia-induced increases in ICAM-1, VCAM-1, MMP-2 andMMP-9 were significantly inhibited in sevo-pre group. Conclusion Repeated preconditioning with sevoflurane confers beneficial effect on ischemic brain injury, partly by suppressing the elevation of proteins with regulatory element κB, such as ICAM-1, VCAM-1, MMP-2 and MMP-9.
出处
《中国临床神经科学》
2013年第5期504-512,共9页
Chinese Journal of Clinical Neurosciences
基金
上海市卫生局青年科研基金项目(编号:20114y128)
国家自然科学基金青年科学基金项目(编号:81200937)
