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1 h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、BP 1 h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 explore changes of NF - κB and its inhibitory protein (IκB) in infection - induced cerebral edema, and to determine whether the protective effect of baicalin on infection - induced cerebral edema was related to the inhibitory effect on NF - κB activation and IκB degradation. Methods Forty - five healthy Sprague- Dawley (SD) rats were randomly assigned into three groups: the normal saline group (NS), the pertussis bacilli group (PB), and the baicalin - treated group (BC). In the BC group, baicalin was administered intraperitoneally every 4 hours from the first hour after the injection of pertussis bacilli. Electrophoretic mobility shift assay (EMSA) was performed on the nuclear extracts to detect the activity of NF - κB and Western blot analysis was performed to detect the expression of IκB - α. Results There was no significant NF- κB activation in the NS group. In the PB gruop, at 1-hour, the levels of NF- κB activation were similar to those in the NS group. In the PB group, at 2 hours, NF -κ B started to be activated. The activity of NF - κB reached the highest level in the PB group at 24 hours. The expression of IκBα began to decrease in the PB group at 2 hours and reached the lowerest level in the PB group at 24 hoars. There was no significant inhibitory effect on NF- κB activity and IκB - α degradation in the BC group at 1 hour. In the BC group, at 2 hours, 4 hours, 8 hours and 24 hours, the activities of NF - κB were lower than those in the relevant PB groups, and the expressions of IB were higher than those in the relevant PB groups. Conclusions NF - κB is strongly activated in infection-induced cerebral edema by pertussis bacilli. The elevation of NF - κB may be a key factor that induces brain edema. The protective effect of baicalin on infection - induced cerebral edema may be associated with the ichbitory effect on NF - κB, activation and IκB degradation.