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目的 探讨地塞米松预处理对新生大鼠缺氧缺血后脑内NF κB活性及神经细胞凋亡的影响。方法 4 2只新生大鼠随机分为 5组 ,即正常对照组 (n =8) ,假手术组 (n =8) ,缺氧缺血组 (HIBD ,n =8) ,地塞米松治疗组 (DEX ,n =9)及地塞米松预处理组 (P DEX ,n =9)。于缺氧缺血 (HI)后 72h取脑 ,以Western印迹法检测脑组织中NF κB抑制蛋白IκBα表达 ,TUNEL法检测细胞凋亡 ,免疫组织化学法检测NF κB亚基p6 5核移位情况 ,免疫荧光双标法检测P6 5核移位与细胞凋亡共表达。结果 与正常对照组和假手术组比较 ,HIBD组及DEX组 p6 5阳性细胞及TUNEL阳性细胞数明显增加 (P <0 .0 1) ,IκBα蛋白表达明显减少 (P <0 .0 1)。P DEX组也可见p6 5阳性细胞及TUNEL阳性细胞表达 ,但较HIBD组及DEX组明显减少 (P <0 .0 1) ,而IκBα蛋白表达明显增多 (P<0 .0 1)。直线回归分析显示 ,在HIBD组中NF κB的活化与缺氧缺血后神经细胞凋亡密切相关 (r =0 .775 ,P <0 .0 1)。结论 NF κB的活化与缺氧缺血后神经细胞凋亡密切相关。DEX预处理对缺氧缺血性脑损伤的保护作用可能与抑制NF κB的活化 ,减少细胞凋亡有关。
Objective To investigate the effect of dexamethasone preconditioning on NF κB activity and neuronal apoptosis in neonatal rats after hypoxic-ischemic brain damage. Methods 4 2 neonatal rats were randomly divided into 5 groups: normal control group (n = 8), sham operation group (n = 8), hypoxic ischemic group (HIBD, n = 8), dexamethasone treatment group (DEX, n = 9) and dexamethasone pretreatment group (P DEX, n = 9). The brain was taken at 72h after hypoxia-ischemia (HI), the expression of NFκB inhibitor IκBα was detected by Western blotting, the apoptosis was detected by TUNEL method, and the nuclear translocation of NFκB subunit p6 was detected by immunohistochemistry Immunofluorescence double-labeled method was used to detect nuclear translocation of P6 5 and co-expression of apoptosis. Results Compared with normal control group and sham operation group, the number of p6 5 positive cells and TUNEL positive cells in HIBD group and DEX group were significantly increased (P <0.01), and the expression of IκBα protein was significantly decreased (P <0.01). The expression of p65 positive cells and TUNEL positive cells in P DEX group was also significantly lower than that in HIBD group and DEX group (P <0.01), while the expression of IκBα protein was significantly increased (P <0.01). Linear regression analysis showed that activation of NF-κB in HIBD group was closely related to apoptosis of neurons after hypoxic-ischemic (r = 0.775, P <0.01). Conclusion The activation of NF κB is closely related to the apoptosis of nerve cells after hypoxia and ischemia. The protective effect of DEX pretreatment on hypoxic-ischemic brain damage may be related to the inhibition of NF κB activation and cell apoptosis.