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作 者:吕松岑[1] 王新涛[1] 关德宏[1] 韩竹[1] 夏双印[1] 孙宇一[1]
机构地区:[1]哈尔滨医科大学第二临床医学院手外科,150086
出 处:《中华手外科杂志》2002年第4期239-241,共3页Chinese Journal of Hand Surgery
基 金:黑龙江省自然科学基金资助项目 (D982 7)
摘 要:目的 研究SOD模型配合物MSODa对骨骼肌缺血再灌注后的保护作用及其机制。方法 将 96只Wistar大鼠建立后肢缺血再灌注模型 ,按手术先后随机分为正常对照组 (1组 )、缺血再灌注组 (2组 )、生理盐水组 (3组 )和MSODa组 (4组 )。 2~ 4组分别在缺血 4h后 ,再灌注 1、2、4、8、12h末 ,测定血浆中的丙二醛 (MDA)、骨骼肌组织中的髓过氧化物酶 (MPO) ,白细胞上 β2 整合素 (CD11b/CD18)和骨骼肌血管中细胞间粘附分子 (ICAM ) 1的表达情况及各组的组织学改变。结果 第 2组各时间点MDA、MPO、CD11b/CD18、ICAM 1的表达均较正常对照组显著升高 ,骨骼肌组织的损伤也随再灌注时间的延长而逐渐加重 ,第 4组则表现为上述变化被明显抑制。结论 MSODa通过减少自由基的生成 。Objective To explore the protective effects of SOD-model coordination compound MSODa in skeletal muscle ischemia / reperfusion and its mechanism. Methods The model of hind limb ischemia / reperfusion injury at rats was set up. Ninety-six rats were divided into 4 groups: normal control group (Group Ⅰ),ischemia / reperfusion injury group (Group Ⅱ), normal saline group (Group Ⅲ), MSODa group (Group Ⅳ).The changes of MDA in the plasma ,MPO in the skeletal muscle, CD11b/CD18 on the leukocyte , ICAM-1 in skeletal muscle and the histological changes were studied at 1h, 2h, 4h,8h,12h during reperfusion after ischemia for 4 hours at group Ⅱ, Ⅲ, Ⅳ, respectively. Results Compared to the control group, the expression of MDA, MPO, CD11b/CD18, ICAM-1 were increased evidently in groupⅡ at different intervals. The longer time of reperfusion ,the more serious the injury of skeletal muscle was. In group Ⅳ, the above-mentioned changes were depressed markedly. Conclusions MSODa can inhibit the expression of free radicals and adhesion molecules,consequently resulting in relief of skeletal muscle ischemia-reperfusion injury.
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