【摘要】 【目的】探讨亚低温对新生大鼠缺氧缺血性脑损伤(hypoxic-ischemic brain damage,HIBD)后脑灰质、室周白质的保护作用。【方法】建立新生大鼠HIBD模型,31℃、34℃亚低温全身干预3 h,观察缺氧缺血(hypoxic-ische-mic,HI)后24 h、72 h、7 d脑皮质、海马、室周白质细胞凋亡、p16、bcl-2表达。【结果】1)p16灰度:模型组表达高于假手术组,HI后24 h达高峰,31℃组表达减少,34℃组总表达不减少,但在HI后24 h表达减少,高峰延迟;2)凋亡细胞灰度:与p16结果一致;3)bcl-2灰度:也与p16结果一致,34℃组术后24 h、HI后72 h表达均减少;4)相关关系:p16、凋亡细胞、bcl-2灰度在各脑区表达一致,两两比较,有相关关系(P<0.01)。【结论】新生大鼠HIBD后亚低温干预通过降低p16、bcl-2的表达、减少细胞凋亡或延缓其高峰对脑灰质、室周白质组织起到保护作用。更多还原

【Abstract】 【Objective】 To investigate the protective effects of hypothermia to the grey matter and the periventricular white matter of the brains of the neonatal rats with hypoxic-ischemic brain damage(HIBD).【Methods】 The 7d neonatal rats got the HIBD model.Hypothermias of 31 ℃,34 ℃ were given to them for 3 h immediately after the operation.The degrees of grey of apoptosis,p16,bcl-2 of the cerebral cortex,the hippocampi tissue and the periventricular white matter in the brains of rats was used to observe when 24,72,168 h after the operation.【Results】 1)The degrees of grey of p16: It was higher in the HIBD group than that in the pseuoperation group,the peak was at 24 hours after HI,it was deduced in 31 ℃ group,it was not deduced in 34 ℃group,but the peak was delated.2) The degrees of grey of apoptosis: It was the same as that of p16.3) The degrees of grey of bcl-2: It was the same as that of p16,it were deduced 24,72 hours after HI in the 34 ℃ hypothermia group.4) Correlation: there were the correlation ships(P<0.01) between either two of the degrees of the greys of p16,apoptosis,bcl-2 in all the brain tissues.【Conclusions】 Hypothermia intervention could obviously deduce the express of p16,bcl-2,deduce apoptosis or delate their peaks of neonatal rats,brains with HIBD,so protected their grey matter tissue and the white matter tissue.更多还原