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作 者:吴思荣[1] 王之敏[2] 李向东[2] 祁震宇[2] 黄坚[1] 金钧[1] 惠国桢[2]
机构地区:[1]苏州大学附属第一医院急诊外科,江苏苏州215006 [2]苏州大学附属第一医院神经外科,江苏苏州215006
出 处:《苏州大学学报(医学版)》2007年第5期677-680,F0002,共5页Suzhou University Journal of Medical Science
基 金:国家自然科学基金资助项目(30271325)
摘 要:目的探讨大剂量甲基强的松龙对创伤性脑损伤后神经细胞凋亡的影响。方法SD大鼠70只,随机分为单纯脑损伤组(A组)和脑损伤后应用大剂量甲基强的松龙组(B组),每组35只。Feeney法致伤,B组伤后静脉注射大剂量甲基强的松龙30mg/kg,分别在伤后1、6、24h和2、3、7、14d处死,每组采集伤灶皮层下白质,应用原位缺口末端标记法(TUNEL)检测神经细胞凋亡的变化,免疫组化ABC法检测caspase-3蛋白的表达。结果A、B两组中均发现凋亡细胞和caspase-3阳性表达。伤后2d达峰值时,A、B两组TNUEL阳性凋亡神经细胞数分别为41.54±9.93和20.44±7.09,caspase-3阳性细胞数分别为29.03±4.56和15.77±3.04。两组比较,差异均有高度统计学意义(P<0.01)。结论创伤性脑损伤可导致神经细胞凋亡;大剂量甲基强的松龙能抑制细胞凋亡。Objective To investigate the effect of high dose methylpredinisolone on neural cells apoptosis after acute traumatic brain injury(TBI). Methods Seventy SD rats were divided equally into 2 groups, the brain injury group (group A) and group of post-treatment with high dose methylpredinisolone group (group B). TBI models of rats were developed with Feeney method, high dose methylprednisolone (30 mg/kg) were administered by intravenous injections, the rats were sacrificed at the 1st, 6th and 24th hour and the 2nd, 3rd, 7th and 14th day after injury. The specimens of the injured subcortical white matter were taken for detecting apoptosis of neural cells by TUNEL and caspase-3 protein expression by means of immunohistochemistry. Results Positive expression of apoptotic neural cells and easpase-3 protein existed both in group A and group B. Two days after TBI, the number of TUNEL-positive neural cells was 41.54±9.93 in group A and 20.44±7.09 in group B; the number of easpase-3-positive cells was 29.03±4.56 in group A and 15.77±3.04 in group B. There was a significant difference remained between group A and group B (P〈0.01). Conclusion These results indicate that TBI can induce apoptosis of neural cells and high dose methylprednisolone can inhibit apoptosis after TBI.
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