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机构地区:[1]中国医科大学附属第一医院骨科,沈阳110001
出 处:《中华实验外科杂志》2005年第2期142-143,共2页Chinese Journal of Experimental Surgery
摘 要:目的 探讨基因重组可溶性补体受体I型 (sCR1)对大鼠急性脊髓损伤组织补体固有成分C9及补体调节因子Clusterin表达的影响。方法 采用改良Allen重物打击法制成SD大鼠急性脊髓损伤模型 ,观察sCR1组与生理盐水 (NS)组在伤后 12h、1、3、7、14d时间点脊髓损伤组织中C9和Clusterin表达的部位及时程 ,并采用斜板实验评定两组大鼠的下肢运动功能 ,比较组间差异。结果 sCR1组及NS组在伤后各个时间点脊髓损伤组织中C9、Clusterin表达增强 ,并存在动态变化过程。sCR1组在伤后各个时间点C9表达均明显轻于NS组 (P <0 .0 1) ;sCR1组在伤后 12h、1、3d时间点Clusterin表达明显轻于NS组 (分别为P <0 .0 1、P <0 .0 1、P <0 .0 5 ) ,伤后 7、14d两组间差异无统计学意义。sCR1组在伤后 3、7、14d时间点大鼠下肢运动功能明显优于NS组 (分别为P <0 .0 5、P <0 .0 1、P <0 .0 1)。结论 基因重组sCR1可显著抑制大鼠急性脊髓损伤组织C9和Clusterin的表达 ,可通过抑制补体系统激活机制减轻继发性脊髓损伤。Objective To study the effects of gene recombination soluble complement receptor type I (sCR1) on the expression of C9 and Clusterin in acute spinal cord injuried tissue of rats.Methods SD rat models of acute spinal cord injury were establised by modified Allen's method.The positve expression sites and time phase of C9 and Clusterin were observed in injuried tissue at 12 h,1,3,7 and 14 d after injury in sCR1 group and normal saline group.Motor function of rat lower extremities was evaluated viathe tiltboard experiment and the differences between the two groups were compared.Results The positive expression of C9 and Clusterin was increased in spinal cord injury tissue at each time point after injury with a kinetic course.C9 positive expression in sCR1 group at each time point after injury was obviously less than that in normal saline group (P< 0.01).Clusterin positive expression in sCR1 group was obviously less than that in normal saline group (P< 0.01, P< 0.01, P< 0.05 respectively) at 12 h,1 and 3 d,but no significant difference at 7 and 14 d after injury.Rat motor function in sCR1 group at 3,7 and 14 d was obviously better than that in normal saline group (P< 0.05, P< 0.01, P< 0.01 respectively).Conclusion Gene recombination sCR1 can obviously inhibit the expression of C9 and Clusterin in acute spinal cord injuried tissue.It can relieve secondary spinal cord injury by inhibiting the activation of the complement system.
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