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作 者:孙兵[1] 车晓明[1] 顾士欣[1] 杨德林[1] 刘晓东[1] 张懋狐[2] 郭礼和[2]
机构地区:[1]复旦大学附属华山医院神经外科,上海200040 [2]中国科学院上海生物化学与细胞生物学研究所
出 处:《中华神经外科杂志》2012年第6期615-618,共4页Chinese Journal of Neurosurgery
基 金:国家自然科学基金资助项目(30600577)
摘 要:目的 探讨锌指蛋白A20抑制NF—κB表达对早期脊髓损伤的影响。方法健康雌性C57/BL/6J小鼠随机分成治疗组、对照组和假手术组,建立小鼠脊髓损伤模型,损伤部位即刻应用A20后,采用RT—PCR法和Westernblot法检测A20表达的变化,Westernblot法检测NF—κB表达的变化;TUNEL法检测脊髓损伤区凋亡细胞数;BMS法评价脊髓功能的恢复。结果A20治疗后1h,在治疗局部的脊髓组织内即可检测到A20表达,表达呈逐渐增强趋势;而NF—KB表达量相应逐步降低;治疗后1d,损伤区域内的TUNEL(+)细胞数开始减少,治疗后3周,阳性细胞数显著减少。BMS评分在治疗后1周开始改善,在2、3周,显著高于对照组(P〈0.05)。结论A20可以抑制NF—KB的表达,减少脊髓损伤后的细胞凋亡,促进受损脊髓的功能改善。Objective To investigate the effects of A20 suppressing NF - KB expression on spinal cord injury at early stage. Methods Female C57/BL/6J mice was randomly divided into treatment group, control group and sham group. Immediately after compression lesion in mouse spinal cord injury model, A20 was applied to the damaged tissue by lipsome. RT - PCR and Western blot were employed to detect the expression of A20a ndWestern blot to detect NF - KB. TUNEL method was used to detecte the aptosis of neurocytes in the injuried spinal area. Behavioural recovery was assessed using Bassl Mouse Scale. Results 1 hour after treatment, A20 expression appeared in leisoned tissue and gradually increased, resulted in steady decline of NF - KB activation. The number of TUNEL( + ) cells in injuried region began to decrease 1 day after treatment and significantly in 3 weeks. Compared with control group, BMS of treatment group increased 1 week after treatment and significantly in 2 and 3 weeks ( P 〈 0. 05 ). Conclusions A20 could suppress the NF - KB expression, which would diminish the neural apoptosis and promote funtional recovery after spinal cord injury.
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