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目的探讨核因子－κＢ（ＮＦ－κＢ）及其抑制蛋白（ＩκＢ）在百日咳菌液所致的大鼠感染性脑水肿模型中的变化及黄芩甙对感染性脑水肿的保护作用是否与抑制ＮＦ－κＢ活化和ＩκＢ降解有关。方法健康ＳＤ大鼠４５只随机分成三组：生理盐水对照组（ＮＳ组）；百日咳菌感染性脑水肿模型组（ＰＢ组）；黄芩甙治疗组（ＢＣ组）。ＢＣ组动物从注菌后 １ｈ起每４ ｈ腹腔注射黄芩甙一次。用电泳迁移率改变法（ＥＭＳＡ）检测各组动物脑组织的 ＮＦ－κＢ与靶基因 ＤＮＡ的结合活性，用Ｗｅｓｔｅｒｎ印迹分析法检测各组动物脑组织的 ＩκＢα表达。结果在 ＮＳ组、ＢＰ１ｈ组 ＮＦ－ κＢ活性较弱，ＢＰ ２ ｈ组 ＮＦ－ κＢ活性增加，以后持续升高，并以 ＰＢ ２４ ｈ组活性最强；ＰＢ ２ ｈ组 ＩκＢα表达开始减少，２４ ｈ降到最低。 ＢＣ ２ ｈ，４ ｈ，８ ｈ，２４ ｈ组 ＮＦ－ κＢ活性低于相应 ＰＢ组。黄芩甙组ＩκＢα表达比相应 ＰＢ组增多。结论百日咳菌所致的大鼠感染性脑水肿模型中ＮＦ－κＢ的活性明显增强，ＮＦ－κＢ活化可能参与了感染性脑水肿发病机制。黄芩甙对感染性脑水肿的保护作用可能是通过抑制ＮＦ－κＢ异常活化和ＩκＢα降解起作用的。
Objective To investigate the changes of nuclear factor-κB (NF-κB) and its inhibitory protein (IκB) in the rat model of infectious brain edema induced by pertussis and whether the protective effect of astragalus on infectious brain edema is related to the inhibition of NF. - KappaB activation is related to IKB degradation. Methods Forty-five healthy SD rats were randomly divided into three groups: normal saline control group (NS group), pertussis-infected cerebral edema model group (PB group), and astragalus treatment group (BC group). Animals in the BC group received intraperitoneal injection of jaundice every 4 hours from the time of 1h post-injection. Electrophoretic mobility shift assay (EMSA) was used to detect the binding activity of NF-κB and target gene DNA in brain tissue of each group. The expression of IκBα in brain tissue of each group was detected by Western blot analysis. Results The activity of NF-κB was weak in NS group and BP1h group. The activity of NF-κB was increased in BP 2 h group and then continued to increase. The activity of PB 24 h group was the strongest; the expression of IκBα in PB 2 h group began to decrease 24 h. drop to lowest. The activities of NF-κB in BC 2 h, 4 h, 8 h, 24 h groups were lower than those in the corresponding PB groups. The expression of IκBα in the Astragalus group was higher than that in the corresponding PB group. Conclusion The activity of NF-κB in the model of infectious cerebral edema induced by pertussis was significantly enhanced. Activation of NF-κB may be involved in the pathogenesis of infectious brain edema. The protective effect of Astragalus membranaceus on infectious brain edema may be through inhibition of abnormal activation of NF-κB and degradation of IκBα.