PEP-1-SOD1预处理对脑梗死小鼠顶叶皮质的保护作用

目的 探讨PEP-1-铜,锌超氧化物歧化酶(PEP-1-SOD1)预处理对小鼠顶叶皮质神经元的保护作用.方法 将健康成年昆明小鼠按随机数字表法分为假手术组、模型组、PEP-1-SOD1组,每组各15只.后两组建立永久性大脑中动脉闭塞模型.造模前30min假手术组及模型组腹腔注射生理盐水200 μL,PEP-1-SOD1组注射PEP-1-SOD1 200 μg.24 h后取各组小鼠顶叶皮质,TTC染色测定梗死灶体积,TUNEL染色测定细胞凋亡,黄嘌呤氧化酶法测定SOD1活性,TBA法测定丙二醛(MDA)含量.结果 与模型组相比,PEP-1-SOD1组梗死灶体积明显缩小,凋亡细胞明显减少,SOD1活性明显升高,MDA含量明显下降,比较差异均有统计学意义(P＜0.05).结论 PEP-1-SOD1预处理可有效减轻脑梗死后顶叶皮质缺血损伤.

Protective effect of PEP-1-SOD1 pretreatment on parietal cortex of mice with cerebral infarction

Objective To investigate the neuropretective effect of PEP-1-SOD1 pretreatment on the parietal cortex of mice with cerebral infarction. Methods Healthy Kunming-mice were assigned randomly into sham-operated group, model group and PEP-1-SOD1 precondition group (n=15). And the models of permanent middle cerebral artery occlusion (pMCAO) were established in the later 2 groups.The mice in the sham-operated group and model group were intraperitoneally injected with 200-ul saline and the mice in the PEP-1-SOD1 precondition group were intraperitoneally injected with 200-ug PEP-1-SOD1 fusion protein 30 min before the model inducement, respectively. The parietal cortex was dissected 24 h after the success of model making. Triphenyltetrazolium chloride (TTC) staining was employed to detect the volume of infarction and TUNEL staining was used to detect the cell apoptosis;the content of malondialdehyde (MDA) was measured using the thiobarbituric acid (TBA) method and the activity of SOD 1 was measured by xanthine oxidase method. Results The volume of infarction in the PEP-1-SOD1 precondition group was obviously smaller than that in the model group (P＜0.05).Compared with those in the model group, significantly reduced apoptotic neural cells were noted in the PEP-1-SOD1 precondition group (P＜0.05). Compared with model group, increased activity of SOD1 and decreased level of MDA were found in the cell apoptosis (P＜0.05). Conclusion Precondition with PEP-1-SOD1 fusion protein can efficiently protect the parietal cortex of mice with cerebral infarction.