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目的探讨慢性低氧高二氧化碳对大鼠海马区NFκB的影响及其在海马损伤中的作用。方法采用慢性低氧高二氧化碳肺动脉高压大鼠模型将30只大鼠随机分为正常对照组(NC)、低氧高二氧化碳2周组(2HH)和低氧高二氧化碳4周组(4HH),免疫组织化学法检测海马CA1/3区NFκB的表达,TUNEL法检测海马细胞的凋亡。结果NC组大鼠海马CA1/3区可见NFκB/p65少量表达于胞浆,而模型组可见NFκB/p65在细胞核内有不同程度的表达,与NC组比较有显著性差异(P<0.01),以4周组最明显。模型组大鼠海马CA1/3区细胞凋亡明显增多(P<0.01),也以4周组最明显。结论慢性低氧高二氧化碳能引起大鼠海马区NFκB活化,NFκB活化与大鼠海马神经元凋亡有密切关系。
Objective To investigate the effects of chronic hypoxia and hypercapnia on NFκB in hippocampus of rats and its role in hippocampal lesion. Methods Thirty rats were randomly divided into normal control group (NC), hypoxic-hypercapnic 2-week group (2HH) and hypoxic-hypercapnic 4-week group (4HH) The expression of NFκ B in hippocampal CA1 / 3 region was detected by histochemical method. The apoptosis of hippocampal cells was detected by TUNEL method. Results The expression of NFκB / p65 in the CA1 / 3 region of hippocampus of rats in NC group was small in the cytoplasm. The expressions of NFκB / p65 in the nucleus of the model group were significantly different from those in the NC group (P <0.01) The most obvious 4 weeks group. The apoptosis of hippocampal CA1 / 3 region in model group was significantly increased (P <0.01), also the most obvious in 4-week group. Conclusion Chronic hypoxia and hypercapnia can induce NFκB activation in hippocampus of rats. NFκB activation is closely related to apoptosis of hippocampal neurons in rats.