摘要
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 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-SODI 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-SODI 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.
出处
《现代生物医学进展》
CAS
2011年第13期2423-2426,共4页
Progress in Modern Biomedicine
关键词
脑缺血再灌注
穿透肽-铜
锌超氧化物歧化酶
B细胞淋巴瘤基因-2
Cerebral ischemia-reperfusion
The cell penetrating peptide-copper
Zinc superoxide dismutase
B-cell lymphoma-2