Abstract 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.
