大鼠颅脑损伤后脑组织肿瘤坏死因子-α的变化及药物干预  

Change of tumor necrosis factor-α level in traumatic brain injury rat caused by drug intervention

作　　者：陈兵[1] 彭浩[1] 尹延庆[1] 吴华伟[1] 梁远生[1] 邹新辉[1] 龙霄翱[1] 

机构地区：[1]广东医学院附属医院神经外科,广东湛江524001

出　　处：《中国微侵袭神经外科杂志》2009年第12期563-565,共3页Chinese Journal of Minimally Invasive Neurosurgery

基　　金：2008年广东省医学科研基金项目(编号:A2008484);2008年湛江市科技攻关项目(编号:2008C05006)

摘　　要：目的探讨地塞米松、尼莫地平及血府逐瘀注射液对大鼠颅脑损伤后脑组织肿瘤坏死因子-α(TNF-α)的影响。方法将105只大鼠随机分为空白对照组(5只),假手术组、模型组、地塞米松组、尼莫地平组、血府逐瘀组,各20只;后5组大鼠再按伤后不同时间点(伤后6h、24h、48h、96h)随机均分,每个时间点5只。采用SD大鼠打击伤模型,按相应分组使用地塞米松、尼莫地平和血府逐瘀注射液进行干预,采用免疫组化法检测打击伤后各时间点TNF-α的表达情况。结果造模后各组大鼠脑组织中TNF-α的表达水平均显著高于空白对照组(P<0.01)。在致伤后48h内,地塞米松组TNF-α的表达较模型组稍低,差异无统计学意义(P>0.05);在伤后96h,地塞米松组TNF-α的表达较模型组明显下降(P<0.01)。在不同时间点,血府逐瘀组与尼莫地平组TNF-α表达均较模型组明显下降(P<0.01)。血府逐瘀组TNF-α表达量最低,与尼莫地平组和地塞米松组比较,差异显著(P<0.01)。结论地塞米松的作用具有迟发性,在颅脑损伤早期不能减轻炎症反应而在晚期能减少TNF-α的产生。尼莫地平与血府逐瘀注射液均可减轻颅脑损伤后的继发性炎症反应,且血府逐瘀注射液的效果强于尼莫地平。Objective To investigate the effects of dexamethasone, nimodipine and Xuefuzhuyu injection on tumor necrosis factor-α （TNF-α） levels in traumatic brain injury rat. Methods One hundred and five rats were randomly divided into 6 groups： blank control group （n = 5）, sham-operated group （n = 20）, model group （n = 20）, dexamethasone group （n = 20）, nimodipine group （n = 20）, Xuefuzhuyu group （n = 20）. The expressions of TNF-α were assayed by immunohistochemistry at 6, 24, 48, 96 h after brain injury in all the groups but blank control group, 5 rats for each time point. Results The expressions of TNF-α were increased significantly in the rat model groups compared with the blank control group （P 〈 0.01）; the expressions of TNF-α in dexamethasone group was slightly lower in 48 hours compared the model group, but no statistical significance was found between them （P 〉 0.05）. However, the expression of TNF-α in dexamethasone group was significantly decreased 96 h after the injury compared with model group （P 〈 0.01）. The expressions of TNF-α in nimodipine group and Xuefuzhuyu group at different time points were all significantly decreased compared with model group （P 〈 0.01）; the expression of TNF-α was lowest in Xuefuzhuyu group, and there existed a significantly differences compared with nimodipine group and dexamethasone group （P 〈 0.01）. Conclusion Dexamethasone has a characteristic of delayed dominance, which can significantly decrease expression of TNF-α in late stage of brain injury but no effects on inflammatory reaction in early stage. Xuefu.zhuyu and nimodipine all can relieve secondary inflammatory reaction, and effect of Xuefuzhuyu is superior to nimodipine.

关 键 词：颅脑损伤 肿瘤坏死因子 大鼠 

分 类 号：R651.15[医药卫生—外科学] R-332[医药卫生—临床医学]