前列腺素E_1对缺血再灌注脑损伤的保护作用

Protective effect of prostaglandin E_1 on cerebral ischemia reperfusion injury

目的:探讨前列腺素E1(PGE1)对缺血再灌注脑损伤的保护作用。方法:采用线栓法复制大鼠局灶性脑缺血再灌注模型。缺血60min,再灌注24h对每只动物进行神经症状评分后,断头取脑,并进行脑梗死体积,脑含水量测定及病理学捡查。结果:①缺血再灌注模型组出现典型神经缺损症状,而PGE1剂量组均能改善大鼠神经功能障碍,其行为评分与模型组相比差异有显著性意义(P<0.05)。②缺血再灌注模型组脑梗死体积百分比高达(28.40±1.83)%,而PGE1中、高剂量组脑梗死体积百分比明显缩小(10.25±2.77)%,(12.90±2.58)%,与模型组相比差异有显著性意义(P<0.05)。③缺血再灌注模型组栓塞侧脑含水量明显增加,为(83.03±0.61)%,而PGE1三剂量组脑含水量均低于模型组,为(79.93±0.70)%,(79.67±1.12)%,(80.26±1.63)%,两者相比差异有显著性意义(P<0.05)。④缺血再灌注模型组脑组积病理形态学捡查可见;大量神经细胞固缩坏死,重度脑水肿,部分可见软化灶形成,而PGE13剂量组脑水肿及神经细胞坏死程度均明显减轻结论:PGE1能减轻脑缺血再灌注所致的组织损伤,发挥保护作用。

AIM:To investigate the effect of prostaglandin E1(PGE1) in protecting cerebral ischemia reperfusion injury. METHODS:Cerebral ischemia reperfusion injury was induced and rat models of foc al cerebral ischemia reperfusion were established.All the rats were evaluated wi th the neural symptom scoring after 60-minute ischemia and 24-hour reperfusion . Then their brains were taken out after decapitation. The infarct volume and wa ter content were measured and pathological examination was performed. RESULTS:① Typical neurological defect symptoms were observed in the ischemia reperfusion model group, while the neurological dysfunction could be improved i n the PGE1 groups of different doses, and the scores were significantly differen t from those in the model group (P< 0.05).②The percentage of infarct volume in the middle and high dose PGE1 groups was obviously reduced[(10.25±2.77)% and (12.90±2.58)%],significantly different from that in the model group (28.40±1. 83)%](P< 0.05).③ Brain water content in the model group was increased obvious ly (P< 0.05).③ Brain water content in the model group was increased obvious ly [(83.03±0.61)%],significantly higher than those in the three PGE1 groups [( 79.93±0.70)%,(79.67±1.12) % and (80.26±1.63) %](P< 0.05).④ The results of pathological examination showed that there were a great amount of pyknosis an d necrosis neural cells, wide-ranging cerebral edema and partial formation of m alacia focal in the model group, while the degrees of cerebral edema and neural cell necrosis were obviously relieved in the PGE1 groups of 3 doses. CONCLUSION:PGE1 can reduce the tissue damage induced by cerebral ischemia repe rfusion,and plays its protective role.