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目的 探讨新生大鼠缺氧缺血性脑损伤 (HIBD)后脑内 μ calpain的活化、其他相关因子表达变化的时程及相互关系 ,进一步研究HIBD的发病机制。方法 HIBD模型采用改良的Rice法。应用Westernblot法半定量测定缺氧缺血 (HI)后 0、1、2、4、12和 2 4h大脑皮层和海马μ calpain、c Fos、c Jun、HSP70和HSP2 7的表达。蛋白浓度测定采用改良的Bradford法。结果 新生大鼠HI后 μ calpain裂解为 76和 80两个片段 ,两者比值在HI后显著提高 ,以海马更为明显 ,其中皮层在 2 4h、海马在 12h达到高峰。c Fos在HI后 2～ 12h海马显著高于皮层 (P <0 0 5 ) ,2 4h海马却低于皮层 (P <0 0 5 ) ;c Jun则 0～ 1h海马高于皮层 (P <0 0 5 ) ,4h以后皮层均高于海马 (P <0 0 5 ) (其中 12h差异无显著意义 )。c Fos和c Jun在HI后呈上升趋势 ,无论皮层或海马均在 2～ 4h达到高峰 ,以后渐下降 ,但 2 4h仍高于正常对照组。与对照组相比 ,c Fos在 1,2 ,4 ,12和 2 4h差异有显著意义 (P <0 0 5 ) ;c Jun在 0 ,1,2 ,4 ,12和 2 4h差异有显著意义 (P <0 0 5 )。HSP70在HI后 0h皮层显著高于海马 (P <0 0 5 ) ,1h海马显著高于皮层 (P <0 0 5 ) ,4h后皮层又均高于海马 (P <0 0 5 ) ;HSP2 7则HI后 1～ 2 4h海马均显著高于皮层 (P <0
Objective To investigate the activation of μ calpain in neonatal rats after hypoxic-ischemic brain damage (HIBD) and the correlation between the expression of other related factors and the pathogenesis of HIBD. Method HIBD model uses a modified Rice method. Semi-quantitative Western blotting was used to detect the expression of μ calpain, c Fos, c Jun, HSP70 and HSP27 in the cerebral cortex and hippocampus at 0, 1, 2, 4, 12 and 24 hours after hypoxia-ischemia (HI) Protein concentration was determined using a modified Bradford method. Results μ calpain was cleaved into two fragments of 76 and 80 in neonatal rats, the ratio of them increased significantly after HI, especially in hippocampus. The cortex peaked at 24 h and hippocampus at 12 h. c Fos was significantly higher in hippocampus than in cortex 2 ~ 12h after HI (P <0.05), but lower in hippocampus 24h than in cortex (P <0.05); c Jun was higher than cortex in 0 ~ 1h 0 5). After 4 hours, the cortex was higher than that of the hippocampus (P <0 05) (no significant difference 12h). c Fos and c Jun showed an upward trend after HI, both in the cortex or hippocampus reached the peak in 2 ~ 4h, then gradually decreased, but 24 h still higher than the normal control group. Compared with the control group, c Fos had significant difference at 1, 2, 4, 12 and 24 hours (P <0.05); c Jun had significant difference at 0, 1, 2, 4, 12 and 24 hours (P <0 05). The level of HSP70 in hippocampus at 0h after HI was significantly higher than that in hippocampus (P <0.05), hippocampus at 1h was significantly higher than that at cortex (P <0 05), and at 4h later the cortex was higher than that at hippocampus (P <0.05) The hippocampus of 1 ~ 24 h after HI was significantly higher than that of the cortex (P <0