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目的 研究新生大鼠脑缺氧缺血 (HI)后TGF - β1表达和神经细胞凋亡的变化规律 ,探讨新生儿缺氧缺血脑损伤的发病机制。方法结扎新生 7d龄SD大鼠左颈总动脉后 ,吸入8%浓度氧 2h ,建立HIBD模型。应用苏木素 -伊红 (HE)染色、原位缺口末端标记 (TUNEL)及SP免疫组化方法检测新生大鼠HI后存活不同时间大脑皮质和海马TGF - β1的表达及神经细胞凋亡的情况。结果缺氧缺血后 8h ,大脑皮质和海马出现TGF - β1的表达 ,缺氧缺血后 12h和 4 8h ,TGF - β1出现两次表达高峰 ,神经细胞凋亡高峰为缺氧缺血后 2 4h,晚期表达TGF- β1的免疫阳性细胞与凋亡细胞均出现在缺血半暗带内。 结论缺氧缺血引起了TGF - β1的表达增强 ,TGF - β1的表达可能通过对神经细胞凋亡的调控 ,参与缺氧缺血后神经细胞的修复
Objective To study the changes of TGF - β1 expression and neuronal apoptosis after hypoxic - ischemic brain damage (HI) in neonatal rats and to explore the pathogenesis of neonatal hypoxic - ischemic brain damage. Methods After the left common carotid artery of neonatal 7d SD rats was ligated, 8% oxygen was inhaled for 2 hours to establish HIBD model. The expression of TGF - β1 in cerebral cortex and hippocampus and the apoptosis of neurons were detected by hematoxylin - eosin (HE) staining, TUNEL and SP immunohistochemistry. Results The expression of TGF - β1 in cerebral cortex and hippocampus appeared at 8 h after hypoxic - ischemic insult. The expression peak of TGF - β1 appeared at 12 h and 48 h after hypoxia - ischemia, and the peak of neuronal apoptosis was hypoxia - ischemia 2 4h, the late expression of TGF-β1-positive cells and apoptotic cells were seen in the ischemic penumbra. Conclusions Hypoxia - ischemia causes the expression of TGF - β1 to be enhanced. The expression of TGF - β1 may be involved in the repair of nerve cells after hypoxia - ischemia by regulating the apoptosis of nerve cells