【摘要 】 目的 研究Bc1-2蛋白和Bax蛋白在新生儿缺氧缺血性脑损伤(HIBD)中的表达，以及与细胞凋亡的关系。 方法 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)。 结果 新生大鼠HIBD时细胞凋亡与坏死并存，但以凋亡为主。Bcl-2和Bax在正常新生大鼠脑内广泛表达(+～)；缺氧缺血(HI)后脑病变处Bcl-2免疫强度明显下降(-～+)；Bax的免疫强度也减弱，其中可见散在分布的阳性凋亡细胞；HI后Bcl-2与Bax的比例下降。 结论 Bcl-2可能抑制细胞凋亡，Bax可能诱发细胞凋亡。

     The Study on TheExpression of Bcl-2 and Bax Proteins after Hypoxic-Ischemic Brain Damage in Neonatal Rat

SUN Guilian,HAN Yukun.Department of Pediatrics, 1st University Hospital, China Medical University, Shenyang 110001

【Abstract 】 Objective Toassess the expression of Bcl-2 and Bax proteins in brain after hypoxic-ischemic braindamage (HIBD) as well as the relationship with apoptosis in the neonate. Methods TheHIBD model was produced with 7-day-old wistar rats. The expression of Bcl-2 and Baxproteins as well as the relationship with apoptosis after HIBD in the neonatal rats weredetermined by immunohistochem and terminal deoxynucleotidyl transferase mediated dUTP-biotin nick end labelling (TUNEL) staining. Results Apoptosis coexisted withnecrosis after HIBD by TUNEL, but apoptosis was a major form of cell death. Bcl-2 and Baximmunostaining ranged from weak to intense(+～) in the brain of normal neonatal rat. After hypoxia-ischemia(HI),a decrease or absence in immunoreactivity for Bcl-2 in apoptotic andnecrotic neurons was observed, and a decrease in immunostaining for Bax was observed inthe infarcted areas.Among them, there were a few scattered strong positive apoptoticcells. Conclusion Overexpression of Bcl-2 protects cell from apoptosis, but Bax mayfunction as a cell death effector protein.

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