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作 者:陈云丰[1] 曾炳芳[1] 张惠箴[1] 刘亮[1] 周健华[1]
机构地区:[1]上海第六人民医院
出 处:《上海医学》2002年第z1期2-4,共3页Shanghai Medical Journal
基 金:上海市卫生局青年科研基金资助项目 (编号13 10 14 1/2 7)
摘 要:目的 建立腰神经根病的动物模型 ,探讨大鼠腰神经根损伤后脊髓神经胶质细胞激活和细胞因子表达。方法 根据对L5神经根不同的处理方法 ,将 74只大鼠分成 4组 :假处理 (sham)组 15例 ,丝线结扎组(silk)组 18例 ,自体髓核 (np)组 18例 ,丝线结扎 +自体髓核 (silk +np)组 2 3例。各组分别于术后 3、7、14、2 8和35d取L5脊髓段作冰冻切片 ,行神经胶质细胞纤维酸性蛋白 (GFAP)和白介素 1β(IL 1β)免疫组化染色。 结果 sham组除术后 3d同侧脊髓后角GFAP和IL 1β反应增高外 ,其余分时段均呈阴性反应 ;silk组、np组和silk +np组与sham组比较 ,前 3者GFAP和IL 1β反应明显强烈 (P <0 .0 1) ;silk组和np组与silk +np组比较 ,后者反应更强烈 (P <0 .0 5 )。结论 silk +np是一种较理想的腰神经根病动物模型 ,神经损伤后可表现出脊髓神经胶质细胞激活和细胞因子表达增高。Objective To establish an ideal and useful animal model for lumbar radiculopathy and detect the spinal nerve glial cells activation and cytokine expression after lumbar radicular injury in rats. Methods According to the differences in treatment of the radicles, 74 rats were divided into four groups: Sham group (n=15), Silk ligation group (n=18), nucleus pulposus group (n=18), Both silk ligation and nucleus pulposus group (n=23). At 3,7,14,28,35 days postoperatively, the rats in each group were perfused with fixative. The L 5 spinal cord segment was harvested and frozen sectioned for immunohistochemistry staining of glial cell and cytokine expression. Results Spinal nerve glial activity and IL-1β expression were not elevated in rats of the sham group in all time points except the postoperative 3 days. Spinal glial activity and IL-1β expression were elevated in rats of the silk ligation group, the nucleus pulposus group and both of them group, there was statistical significance between and those in the sham group and the above three groups(P< 0.01 ); In rats of both silk ligation and nucleus pulposus group, the glial activity and the IL-1β expression were as compared with those in either alone enhanced, there was statistical significance between them (P<0.05).Conclusion A relatively ideal animal model for lumbar radiculopathy can be made by tight tying the radicles with silk and with nucleus pulposus. Radicular injury can cause the glial activation and enhancement of IL-1β expression of the spinal nerve.
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