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出 处:《中华急诊医学杂志》2006年第6期513-515,共3页Chinese Journal of Emergency Medicine
基 金:湖北省科技厅"十五"重点攻关资助项目(2001AA307B)
摘 要:目的研究亚低温状态下,大鼠局灶性脑缺血再灌流后不同时程脑组织中的细胞间黏附分子1(ICAM1),肿瘤坏死因子(TNFα)和白细胞介素1(IL1β)的动态变化,以探讨亚低温对脑缺血再灌流损伤时的保护机制。方法采用大鼠大脑中动脉(MCA)线栓闭塞/再通法建立大鼠局灶性缺血再灌流模型,常温组和亚低温组分别于脑缺血3h再灌流6h、12h、24h、48h、72h时间点断头取脑,假手术组则于再灌流24h断头取脑,进行ICAM1、TNFα和IL1β免疫组化测定;同时在再灌流24h进行神经功能和脑梗死体积的比较。结果(1)亚低温干预可以改善大鼠脑缺血再灌流后的神经功能障碍,缩小脑梗死体积(P<0.01);(2)脑缺血再灌流后,脑缺血灶ICAM1、TNFα和IL1β的表达出现增高趋势,分别在再灌流48h、24h和6h达高峰,与假手术组比较有显著意义(P<0.01);且亚低温干预明显抑制它们的表达(P<0.01)。结论亚低温干预能明显减轻缺血再灌流后脑组织的炎症反应,亚低温对炎症级联反应的抑制可能是其发挥脑保护作用的重要机制之一。Objective To evaluate the protective effect of mild hypothermia against inflammatory cascade reaction in rats during cerebral ischemia and reperfusian. Methods After middle cerebral artery ecclusion (MCAO) for 3 h in rats, the expression levels of ICAM-1, TNF-α and IL-1β in the ischemic regions were determined at different reperfusian time (6 h, 12 h, 24 h, 48 h and 72 h). At 24 h, the cerebral infarction volume and neurologic function were evaluated. In the control, these were assessed at 24 hours repedusion. Results (1) Mild hypothermia could ameliorate neurological deficit score and decrease infarct volume induced by cerebral ischemia and reperfusian. (2) The expression of ICAM-1, TNF-αand IL-1βrose obviously at 6 h after cerebral ischemia-reperfusian, and peaked each at 48 h, 24 h and 6 h. There was significant difference between the various groups and the sham-operative group ( P 〈 0.01 ). Mild hypothermia could reduce the expression of ICAM-1, TNF-α and IL-1β (P〈0.01 ) Conclusion During cerebral ischemia-reperfusian, mild hypothermia could influence the expression of ICAM-1, TNF-α and IL-1β, and play an important role in decreasing the early onset of infiammatory cascade reaction, which might be one of the neuroprotective mechanisms of mild hypothermia.
分 类 号:R743.33[医药卫生—神经病学与精神病学]
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