[Nuclear factor-kappa B activity at the early stage of brain ischemia and reperfusion in mice].

Jin-xiu Li, Jun-wei Deng, Guang-sen Zhang
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Abstract

Objective: To observe the activity of nuclear factor-kappa B(NF-kappa B) during reperfusion after temporary brain ischemia and to evaluate its effect.

Methods: The brain ischemia-reperfusion(I/R) model of mice was established with ligating bilateral common carotid arteries and bleeding for 0.3 ml in the tail. Abnormal nervous symptoms (ANS) were recorded. Immunohistochemical technique was used to detect the activity of NF-kappa B subunit P65 and the inhibitory factor-kappa B alpha(I-kappa B alpha) in cerebral cortex during different periods of ischemia and reperfusion. Their mRNA expressions were also measured by RT-PCR.

Results: NF-kappa B P65 activity significantly increased 30 minutes after the reperfusion, peaking at the 2nd hour, and remaining high within 24 hours (all P < 0.05). But the mRNA expression didn't change much; I-kappa B alpha and its mRNA expression began to decrease at 30 minutes after the reperfusion, peaking at the 2nd hour after the reperfusion (P < 0.05) and then gradually restored. Positive correlation was found between NF-kappa B P65 activity and ANS (P < 0.05), while negative correlation was shown among I-kappa B alpha, its mRNA, and ANS (P < 0.05, respectively).

Conclusion: Both activated NF-kappa B and decreased I-kappa B alpha exist in the neural tissues of mice at the early stage of brain ischemia-reperfusion. The activated NF-kappa B may be involved in the ischemia-reperfusion injury.

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[小鼠脑缺血再灌注早期核因子κ B的活性]。
目的:观察脑暂时性缺血后再灌注时核因子κ B(nf - κ B)的活性并评价其作用。方法:结扎双侧颈总动脉,尾部出血0.3 ml建立小鼠脑缺血再灌注(I/R)模型。记录异常神经症状(ANS)。采用免疫组织化学技术检测缺血再灌注不同时期大鼠大脑皮层nf - κ B亚基P65及κ B α抑制因子(i - κ B α)的活性。RT-PCR检测各组mRNA表达。结果:NF-kappa B P65活性在再灌注后30 min显著升高,在2 h达到峰值,24 h内保持高位(均P < 0.05)。但mRNA表达变化不大;I-kappa B α及其mRNA表达在再灌注后30min开始下降,在再灌注后2h达到峰值(P < 0.05),随后逐渐恢复。NF-kappa B P65活性与ANS呈正相关(P < 0.05), I-kappa B α及其mRNA与ANS呈负相关(P < 0.05)。结论:脑缺血再灌注早期小鼠神经组织中存在nf - κ B活化和i - κ B α降低。活化的nf - κ B可能参与缺血再灌注损伤。
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