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为探讨促甲状腺素释放激素 (TRH)类似物YM1 4673 (YM)对脑缺血损伤保护作用的机制 ,用无损伤小动脉瘤夹夹闭Wistar大鼠大脑中动脉 (MCA)和双侧颈总动脉 (CCAs) 1h ,造成脑缺血再循环模型。大鼠脑冠状切片 (1 0μm)分别进行苏木素 伊红 (HE)染色和免疫组化染色。结果 :缺血 1h再灌 2 4h给药组 (术前 3 0min,ip ,YM 1mg/kg)与缺血组比较大脑皮质神经元降解相对减少。缺血 1h再灌 4h ,缺血组海马结构齿状回及CA4区有强的c fos蛋白样免疫反应 (CFPLI) ,而给药组在上述区域CFPLI相对较低。表明YM对缺血神经元c fos的表达有一定的抑制作用。
To investigate the protective mechanism of thyrotropin-releasing hormone (TRH) analogue YM1 4673 (YM) against cerebral ischemia injury, the middle cerebral artery (MCA) and bilateral neck of Wistar rats were clipped with noninvasive small aneurysm clips. Arteries (CCAs) 1h caused a model of cerebral ischemia recirculation. Cortical coronal sections (10 μm) of the rat brain were stained with hematoxylin (HE) and immunohistochemically. RESULTS: Compared with the ischemic group, the degradation of neurons in the cerebral cortex was relatively decreased in the ischemia-reperfusion group (preoperatively for 30 min, ip, YM 1 mg/kg). After ischemic 1h and reperfusion for 4h, there was a strong cfos protein-like immune response (CFPLI) in the dentate gyrus and CA4 region of the hippocampus in the ischemic group, while the CFPLI in the treated group was relatively low. It was shown that YM has a certain inhibitory effect on the expression of c fos in ischemic neurons.