Objective: Spinal cord ischemia/reperfusion (I/R) injury may lead spinal cord functional impairment and paraplegia, and we want to investigate the protective roll of xenon (Xe) delayed post-conditioning via protein kinase B (Akt) signal pathway activation in spinal cord I/R injury in experimental rats. Methods: A total of 112 male SD rats were divided into 7 groups:①I/R group,②I/R+Xe group,③I/R+wortmannin (PI3K-Akt blocker) group,④I/R+DMSO (solvent) group,⑤I/R+wortmannin+Xe group,⑥I/R+DMSO+Xe group,⑦Sham group.n=16 in each group. The excise function in hind legs of rats were observed at 6, 12, 24, 48 hours after treatment; the survival neuron was examined by Nissl staining and TUNEL staining at 4, 48 hours after treatment, and the protein expression of p-Akt in spinal cord was measured by Western blot analysis. Results: Compared with Sham group, all other groups showed obviously decreased excise function in hind legs of rats with less spinal motor neurons, more apoptosis and lower protein expression of p-Akt at each time point, P<0.05.Compared with I/R group, I/R+Xe group presented increased excise function in hind legs, more spinal motor neurons,less apoptosis and elevated protein expression of p-Akt P <0.05. Compared with I/R+Xe group, I/R+wortmannin+Xegroup indicated decreased excise function in hind legs, less spinal motor neurons, more apoptosis and inhibited proteinexpression of p-Akt, P <0.05. While protein expression level was similar between I/R group and I/R+wortmannin+Xegroup, P >0.05.Conclusion: Xenon delayed post conditioning may protect spinal cord I/R injury via Akt pathway activation inexperimental rats.%目的:探讨蛋白激酶B(Akt)信号通路在氙气延迟后处理对大鼠脊髓缺血再灌注损伤中的作用.方法:建立大鼠脊髓缺血再灌注损伤模型.采用随机数表法将实验动物分为7组(n=16):脊髓缺血再灌注组(I/R组)、脊髓缺血再灌注+氙气延迟后处理组(I/R+Xe组)、脊髓缺血再灌注+PI3K/Akt阻断剂组(I/R+wortmannin组)、脊髓缺血再灌注+阻断剂溶剂二甲基亚砜(DMSO)组(I/R+DSMO组)、脊髓缺血再灌注+PI3K/Akt阻断剂+氙气延迟后处理组(I/R +wortmannin+Xe组)、脊髓缺血再灌注+阻断剂溶剂DMSO+氙气延迟后处理组(I/R+DMSO+Xe组)、假手术组(Sham组).分别于缺血再灌注后6、12、24、48 h观察记录大鼠后肢运动功能,于缺血再灌注后4 h(n=8)和48 h(n=8)行尼氏染色、TUNEL染色检测存活及凋亡指数,行蛋白印迹法(Western blot) 测定脊髓组织中p-Akt蛋白表达.结果:与Sham组相比,其余各组大鼠在各检测时点后肢运动功能评分显著降低,脊髓前角运动神经元存活数量显著减少、凋亡数量显著增加,p-Akt水平显著增高(P<0.05).I/R+Xe组较I/R组大鼠在各检测时点后肢运动功能评分显著增加,脊髓前角运动神经元存活数量显著提高、凋亡数量显著减少,p-Akt水平显著增高(P<0.05).I/R+wortmannin+Xe组较I/R+Xe组大鼠在各检测时点后肢运动功能评分明显下降,脊髓前角运动神经元存活数量显著减少、凋亡数量显著增加,p-Akt水平显著降低(P<0.05).结论:氙气延迟后处理通过激活Akt信号通路对大鼠脊髓缺血再灌注损伤起到保护作用.
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