新生鼠缺氧缺血脑损伤TGF-β1表达与神经细胞凋亡

The expression of TGF-β1 and neurons apoptosis in injured brain tissue of neonatal rats caused by hypoxia and ischemia

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 。

AimTo study the sequential changes of the expression of TGF-β 1 and neurons apoptosis following hypoxia and ischemia(HI)in the cerebral cortex and hippocampus of the neonatal rat brain for further investigating the pathogenesis of neonatal cerebral injury. MethodsAn animal model of neonatal hypoxic and ischemic brain damage was set up by ligating the unilateral carotid artery of 7-day-old SD rats and keeping the rats in a hypoxic environment (8% oxygen) for 2 hours. The rats' brain tissues were collected at different time. Hematoxylin-eosin staining, terminal deoxynucleotidyl transferase mediated dUTP-biotin nick end labeling(TUNEL) staining and immunohistochemistry was used to detect neurons apoptosis and the expresson of TGF-β1 in the cerebral cortex and hippocampus, respectively. ResultsOur results showed that the expresson of TGF-β1 in the cerebral cortex and hippocampus began at 8 hours, peaked separately at 12 hours and 48 hours after hypoxia and ischemia. No apoptotic signals could be found in the control group. Neuron apoptosis 24 hours after hypoxia and ischemia was much more than that in the control group. Conclusion These results indicate that the expressed ion increase of TGF-β1 may be induced by neonatal hypoxia and ischemia. It indicated that TGF-β1 may regulate the apoptosis, and play a very important role in preventing neurons from injury following cerebral hypoxia and ischemia.