亚低温对大鼠局灶性脑缺血ICAM-1和TNF-α表达的影响

目的:脑缺血后ICAM-1和TNF-α的表达增加。降低ICAM-1和TNF-α的表达和亚低温对缺血性脑卒中具有神经保护作用。本研究的目的在于观察亚低温对大鼠局灶性脑缺血ICAM-1和TNF-α表达的影响,并探讨亚低温对脑缺血性损害的神经保护作用机制。方法:采用栓线法阻断大鼠一侧大脑中动脉制作局灶性脑缺血动物模型,设实验组和对照组,分别置于冰毯机上和常温操作台上,使其肛温分别保持在34℃±0.5℃和37℃±0.5℃。12h后断头取脑,采用免疫组化方法检测缺血区ICAM-1阳性血管数目和采用双抗夹心酶联免疫吸附法(ELISA)测定血清TNF-α水平。结果:实验组ICAM-1和TNF-α的表达较对照组下降。结论:亚低温可降低大鼠局灶性脑缺血的ICAM-1和TNF-α的表达,推测亚低温降低ICAM-1和TNF-α的表达为亚低温减轻脑缺血性损害的神经保护作用机制之一。

Effect of mild hypothermia on the expression of ICAM-1 and TNF-alpha after MCAO in rats

Object: The expression of intercellular adhesion molecule-1 (ICAM-1) and tumor necrosis factor-alpha (TNF-alpha) is increased after cerebral ischemia. Mild hypothermia and reducing the expression of ICAM-1 and TNF-alpha are neuroprotective. The chief aim in this study was to investigate whether mild hypothermia is associated with the expression of ICAM-1 and TNF-alpha at 12h after middle cerebral artery occlusion (MCAO) in Sprague-Dawley rats and the neuroprotective mechanism of mild hypothermia in treating ischemic stroke. Methods: Sixty male Wistar rats weighing 280-320 g were randomly assigned to the experiment group and the control group. We made infarct models of rats with thread embolism. The rectal temperature of the experiment group was controlled at 34. 0℃+0. 5℃ after MCAO. The rectal temperature of the contrl group was controlled at 37. 0℃ +0. 5℃ after MCAO. Results: Immunohistochemistry showed that ICAM- 1 positive microvascular endothelial cells of murine brain in the experiment group are lower than that in the control group. The serum levels of TNF-alpha measured by enzyme-linked immunosorbent assay(ELISA) in the experiment group are lower than that in the control group. Conclusion: Mild hypothermia can reduce the expression of ICAM-1 and TNF-alpha after cerebral ischemia. We presume reducing the expression of ICAM-1 and TNF-alpha is one of the neuroprotective mechanism in treating ischemic stroke by using mild hypothermia.