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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 investigate the dynamic changes of ICAM1, TNFα and IL1β in brain tissue after focal cerebral ischemia and reperfusion in mild hypothermia rats Changes in order to explore the mechanism of hypothermia on cerebral ischemia-reperfusion injury. Methods The rat models of focal ischemia-reperfusion were established by occlusion / reperfusion of middle cerebral artery (MCA) rats. The rats in normal temperature group and mild hypothermia group were reperfused for 6h, 12h, 24h, 48h , The brain was decapitated at 72h, and the sham operation group was subjected to decapitation at 24 hours after reperfusion. The levels of ICAM1, TNFα and IL1β were determined by immunohistochemistry. Meanwhile, the volume of neurological function and cerebral infarction were compared 24h after reperfusion. Results (1) Mild hypothermia can improve neurological dysfunction after cerebral ischemia-reperfusion in rats and decrease the volume of cerebral infarction (P <0.01). (2) After cerebral ischemia-reperfusion, the levels of ICAM1, The expression of IL1βincreased, which peaked at 48h, 24h and 6h after reperfusion, respectively. Compared with the sham-operated group, the expression of IL-1β was significantly increased (P <0.01), and mild hypothermia intervention significantly inhibited the expression of IL1β (P <0.01). Conclusion Mild hypothermia can obviously reduce the inflammatory reaction in the brain tissue after ischemia-reperfusion. The inhibition of the inflammatory cascade by mild hypothermia may be one of the important mechanisms of cerebral hypothermia.