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【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。
【Objective】 To investigate the protective effects of mild hypothermia on gray matter and periventricular white matter in neonatal rats with hypoxic-ischemic brain damage (HIBD). 【Method】 HIBD model of neonatal rats was established. After systemic hypothermia at 31 ℃ and 34 ℃ for 3 h, the cerebral cortex, hippocampus, and hippocampus were observed at 24 h, 72 h and 7 d after hypoxic-ischemic (HI) Peripheral leukocyte apoptosis, p16, bcl-2 expression. 【Results】 1) The gray level of p16 in model group was higher than that in sham-operation group, reached the peak at 24 h after HI, decreased at 31 ℃, but decreased at 34 ℃, but decreased at 24 h ; 2) The gray level of apoptotic cells was consistent with the result of p16; 3) The gray level of bcl-2 was also consistent with the result of p16. The expression of p16 Apoptotic cells, bcl-2 gray-scale expression in the brain area consistent, any pair of comparison, there is a correlation (P <0.01). 【Conclusion】 Mild Hypothermia in neonatal rats after HIBD can protect the gray matter and periventricular white matter tissue by decreasing the expression of p16 and bcl-2, decreasing apoptosis or delaying its peak.