胰岛素对缺氧/复氧神经元上的HMGB1、NF-κB表达的影响

Effect of insulin on HMGB1 and NF-κB expressed in cultured neurons after hypoxia/reoxygenation

目的探讨胰岛素(insulin,In)对缺氧/复氧诱导新生大鼠皮质神经元损伤的保护作用及其机制。方法将培养7 d的大鼠皮质神经元随机分为3组,A组为正常对照组,B组单纯采用缺氧/复氧(H/R),C组采用In预处理加H/R,各组在H/R后0、3、6、12、24h各时间点,以TUNEL比较各组凋亡细胞,免疫组化比较各组高迁移率族蛋白B1(high mobilitygroup protein box 1,HMGB1)、核因子κB(nuclear factorκB,NF-κB)表达。结果①B组凋亡神经元明显多于A组,C组显著少于B组,3组比较差异有统计学意义。②B组HMGB1、NF-κB的表达较正常对照组明显增加,C组HMGB1、NF-κB表达较B组明显减少。结论In可使H/R后神经元HMGB1、NF-κB表达降低,抑制神经元凋亡,这可能是其脑保护作用的机制之一。

Objective To explore the protective effects of insulin（In） on injured neurons induced by H/R and the mechanisms of that. Methods Cortical neurons cultured for 7 days were randomly divided into A （normal control group）, B （H/R a- lone）, C （pretreatment with In, and H/R） 3 groups. Then the apoptotic neurons were counted by TUNEL, and the expressions of HMGB1, NF-κB were observed by immunocytochemical technique on 0.3.6.12.24h time-points after H/R. Results （1）The apoptotic neurons in group B were more than those in group A, and they were less in group C than those in group B. （2） The expressions of HMGB1 and NF-κB were increased in group B than those in group A. And they were lower in group C than those in group B. Conclusion In could decrease the expressions of HMGB1 and NF-κB, and inhabit neuronal apoptosis after H/ R, this may be one of the mechanisms in which In exerts its neuro-protection.