论文部分内容阅读
为研究 Bcl- 2和 Fas配体 (Fas L )基因蛋白在新生儿缺氧缺血性脑损伤 (HIBD)中的表达及与细胞凋亡的关系 ,将新生 7日龄 Wistar大鼠制成 HIBD模型 ,应用免疫组织化学 - SP法及原位缺口末端标记 (TUNEL )研究 Bcl- 2和 Fas L蛋白在新生大鼠及缺氧缺血 (HI)后脑中表达及与凋亡的关系。结果示新生大鼠 HIBD时凋亡与坏死并存 ,以凋亡为主。Bcl- 2免疫蛋白在正常新生大鼠脑内广泛表达 (+～ + + + + ) ;HI后脑病变处 Bcl- 2免疫强度明显下降 (-～ + ) ;Fas L蛋白在正常新生大鼠脑内呈不表达或弱表达 (-～ + + ) ,HI后病变部位散在分布阳性凋亡细胞。由此可见 HI后 Bcl- 2与 Fas L的比例下降有助于 HI后脑细胞的凋亡
To investigate the expression of Bcl-2 and Fas L gene proteins in neonatal hypoxic-ischemic brain damage (HIBD) and their relationship with apoptosis, newborn 7-day-old Wistar rats were made into HIBD The expression of Bcl-2 and Fas L proteins in the brain of neonatal and hypoxic-ischemic (HI) rats and the relationship with apoptosis were studied by immunohistochemical SP method and TUNEL. The results showed that neonatal rats HIBD apoptosis and necrosis coexist, mainly apoptosis. Bcl-2 protein was widely expressed in normal neonatal rat brain (+ ~ + + +); Bcl-2 immunoreactivity was significantly decreased in HI rats (~ +); Fas L protein was detected in normal neonatal rat brain No or weakly expressed (- ~ + +), positivly distributed positive apoptotic cells in the lesion site after HI. This shows that the ratio of Bcl-2 and Fas L decreased after HI contribute to the apoptosis of brain cells