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目的：观察细胞穿透肽- 铜，锌超氧化物歧化酶（PEP-1-SOD1）预处理对大鼠局灶性脑缺血再灌注损伤的改善作用及其脑保护机制。方法：线栓法建立大鼠局灶性脑缺血6h 后再灌注损伤模型，进行神经行为评分，并通过HE 染色在光镜下观察神经细胞损伤变化，免疫组化法检测B 细胞淋巴瘤基因-2(B-cell lymphoma-2，Bcl-2)蛋白的阳性表达。结果：盐水对照组（缺血再灌注组或模型组）神经障碍显著高于假手术组（P＜0.05），与模型组相比，PEP-1-SOD1 预处理组可降低神经障碍评分（P＜0.05）；光镜下，假手术组神经细胞结构正常，PEP-1-SOD1 预处理组和缺血再灌注组均有不同程度的缺血再灌注损伤，PEP-1-SOD1 预处理组较缺血再灌注组损伤轻；假手术组Bcl-2 蛋白表达极弱，缺血再灌注组和PEP-1-SOD1 预处理组在脑缺血再灌注后6h 在缺血半暗带周围出现Bcl-2 蛋白阳性表达，24h 达到高峰，48h 表达开始减少。与假手术组相比，PEP-1-SOD1 预处理组和缺血再灌注组Bcl-2 蛋白阳性细胞数显著增多（P＜0.05）；与缺血再灌注组相比，PEP-1-SOD1 预处理组Bcl-2 蛋白阳性细胞数显著增多（P＜0.05）。结论：PEP-1-SOD1 对大鼠局灶性脑缺血再灌注损伤有保护作用，PEP-1-SOD1 可通过上调Bcl-2 蛋白的表达发挥脑保护作用。

英文摘要:

Objective: To observe the cell penetrating peptide-copper, zinc superoxide dismutase (PEP-1-SOD1) preconditioning on focal cerebral ischemia-reperfusion injury in the brain and its protective mechanism to improve. Methods: Suture technique in rats 6h after focal cerebral ischemia-reperfusion injury model, the neural behavior scores, and by HE histological changes of nerve cell damage, immune staining B-cell lymphoma gene-2 (B-cell lymphoma-2, Bcl-2) protein expression. Results:Saline control group (ischemia -reperfusion group or model group) neurological disorders were significantly higher than sham operation group (P＜0.05), compared with model group, PEP-1-SOD1 pretreatment could reduce the neurological deficits score (P＜0.05 ); light microscope, the sham operation group of neurons was normal, PEP-1-SOD1 pretreatment group and the ischemia reperfusion group had different levels of ischemia-reperfusion injury, PEP-1-SOD1 pretreatment group than in the ischemia-reperfusion group of light damage;sham group the expression of Bcl-2 protein in very weak, ischemia-reperfusion group and PEP-1-SOD1 pretreatment group 6h after cerebral ischemia-reperfusion in the ischemic penumbra appears around the Bcl-2 protein expression, 24 h reached a peak, 48h expression started to decrease; compared with the sham group, PEP-1-SOD1 pretreatment group and the ischemia-reperfusion group Bcl-2 protein positive cells was significantly increased (P＜0.05); compared with the ischemia-reperfusion group, PEP-1-SOD1 pretreatment group Bcl-2 protein positive cells was significantly increased (P＜0.05). Conclusions: PEP-1-SOD1 on focal cerebral ischemia-reperfusion injury had a protective effect, PEP-1-SOD1 could increase the expression of Bcl-2 proteins play a role in cerebral protection.

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