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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。
Objective: To observe the effect of PEP-1-SOD1 pretreatment on focal cerebral ischemia-reperfusion injury in rats and its mechanism of cerebral protection. Methods: The reperfusion injury model was established 6h after focal cerebral ischemia in rats. The neurobehavioral scores were scored. The changes of neuronal damage were observed under light microscope by HE staining. The B cell lymphomas -2 (B-cell lymphoma-2, Bcl-2) protein expression. Results: Compared with the sham group, the neurological deficit in the saline control group (ischemic reperfusion group or model group) was significantly higher than that in the sham operation group (P <0.05). Compared with the model group, the PEP-1-SOD1 preconditioning group reduced the neurological deficit score <0.05). Under the light microscope, the structure of nerve cells in sham operation group was normal, the PEP-1-SOD1 preconditioning group and the ischemia-reperfusion group all had different degrees of ischemia-reperfusion injury, PEP-1-SOD1 pretreatment group Bcl-2 protein expression in sham-operation group was very weak. In ischemic-reperfusion group and PEP-1-SOD1 preconditioning group, Bcl-2 appeared in ischemic penumbra around 6h after cerebral ischemia-reperfusion -2 protein positive expression peaked at 24h, 48h expression began to decrease. Compared with the sham operation group, the number of Bcl-2 positive cells in PEP-1-SOD1 preconditioning group and ischemia-reperfusion group increased significantly (P <0.05). Compared with ischemia reperfusion group, PEP-1-SOD1 Pretreatment group Bcl-2 protein positive cells increased significantly (P <0.05). CONCLUSION: PEP-1-SOD1 has a protective effect on focal cerebral ischemia-reperfusion injury in rats. PEP-1-SOD1 can protect brain through up-regulating Bcl-2 protein expression.