新生大鼠缺氧缺血性脑损伤时Bcl-2和P53蛋白的表达

目的研究Bcl-2的P53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。方法将新生7日龄Wistar大鼠制成HlBD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P53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(+～++++);Hl后脑病变处Bcl-2免疫强度明显下降(-～+);P53蛋白在正常新生大鼠脑内基本无表达;HI后病变部位散在分布阳性凋亡细胞。结论Hl后Bcl-2免疫表达减弱,P53的免疫表达增强,提示Bcl-2可抑制凋亡,P53可能促进凋亡。

Expression of Bcl-2 and P53 Proteins After Hypoxic-lschemic Brain Damage in Neonatal Rat

Aim: To assess the expresion of Bcl-2 and P53 proteins in brain after hypoxic-ischemic brain damage (HIBD) as well as the relationship to apoptosis in the neonate. Methods: The HIBD model was established with 7-old-day Wistar rats. The expression of Bcl-2 and P53 proteins as well as the relationship to apoptosis after HIBD in the neonatal rat were deter- mined by immunohistochemistry and terminal deoxynucleotidyl transferase mediated dUTP-biotin nick end labelling (TUNEL) staining. Results: Apoptosis coexisted with necrosis after HIBD by TUNEL, but apoptosis was a major form of cell death. Bcl-2 immunostaining ranged from week to intense ( - ) in the brain of normal neonatal rat. After hy- poxia ischemia (HI), a decrease or absence in immunoreactivity for Dcl-2 in apoptotic and necrotic neurons was observed. The expression of P53 immunoreactive protein was not detected in the brain of normal neonatal rat, but strong P53-immunoreac- tive was found in apoptotic and necrotic cells. Conclusion: The expression of Bcl-2 decreased. while P53-immunoreative in- creased. Overexpression of Bcl-2 protects cell from apoptosis, but Bax may be function as a cell death effector protein.