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目的:探讨新生大鼠缺氧缺血脑损伤后皮质区细胞间黏附分子-1(ICAM-1)蛋白的表达及辛伐他汀的干预作用。方法:选用144只7日龄SD大鼠,随机分为假手术组、生理盐水组、胞二磷胆碱组、辛伐他汀组,每组又分为0、12、24、48、72 h和7天6个时间点,每个时间点6只,按R ice方法,制作成H IBD模型后,各组分别于即刻及之后的每天同一时刻进行不同的干预,假手术组仅手术游离左侧颈总动脉但不结扎,不再进行缺氧及药物干预等处理。于不同时间点剥取结扎侧脑皮质,免疫组化检测结扎侧脑皮质ICAM-1蛋白的表达,并比较各组之间的差别。结果:阴性对照组未见ICAM-1表达阳性的微血管,假手术组结扎侧皮质区ICAM-1蛋白阳性率均较低,各时间点皮质部位ICAM-1蛋白的表达差异无统计学意义(F=2.434,P>0.05)。生理盐水组、胞二磷胆碱组和辛伐他汀组ICAM-1蛋白表达阳性血管数于缺氧缺血后12 h时开始显著升高,24 h达高峰,然后开始回落,到7天时,生理盐水组和胞二磷胆碱组ICAM-1蛋白表达阳性血管数仍然显著高于假手术组(P<0.01),胞二磷胆碱组、辛伐他汀组于12、24、48、72 h时显著低于生理盐水组,7天时,辛伐他汀组已接近假手术组水平(P>0.05),且72 h、7天时,辛伐他汀组ICAM-1蛋白的表达显著低于胞二磷胆碱组(P<0.05和P<0.01)。结论:辛伐他汀和胞二磷胆碱对新生大鼠缺氧缺血脑损伤有保护作用,机制可能与其调控ICAM-1有关,且辛伐他汀的调控作用更强。
Objective: To investigate the expression of intercellular adhesion molecule-1 (ICAM-1) protein in the cortex after hypoxic-ischemic brain damage in neonatal rats and the intervention of simvastatin. Methods: Seventy-four SD rats of 7 days old were randomly divided into sham operation group, normal saline group, citicoline group and simvastatin group, and each group was divided into 0, 12, 24, 48 and 72 h And 7 days 6 time points, each time point 6, according to R ice method, made into IBD model, each group immediately and after the same time each day for different interventions, sham-operated group only surgery free left Side of the common carotid artery but not ligation, no longer hypoxia and drug intervention and other treatment. The ligation of the cortex was performed at different time points. The expression of ICAM-1 protein in the ligation side of the cortex was detected by immunohistochemistry. The differences among groups were also compared. Results: The negative control group showed no ICAM-1 positive microvessels. The positive rates of ICAM-1 protein in the ligation cortex of sham operation group were lower than those in the sham-operation group, and there was no significant difference in the expression of ICAM-1 protein = 2.434, P> 0.05). The number of ICAM-1 positive neurons in the normal saline group, citicoline group and simvastatin group began to increase significantly at 12 h after hypoxia-ischemia and peaked at 24 h, then began to decline. At 7 days, The number of positive ICAM-1 positive cells in the saline group and the citicoline group was still significantly higher than that in the sham operation group (P <0.01). In the citicoline group and simvastatin group, h, the level of ICAM-1 protein in simvastatin group was significantly lower than that in sham-operated group (P> 0.05) at 7 days, (P <0.05 and P <0.01). CONCLUSION: Simvastatin and citicoline have protective effects on hypoxic-ischemic brain damage in neonatal rats. The mechanism may be related to its regulation of ICAM-1, and the regulation effect of simvastatin is stronger.