Neuroprotective effects of anti-high-mobility group box 1 antibody in juvenile rat hippocampus after kainic acid-induced status epilepticus.

High-mobility group box 1 (HMGB1) is a potent cytokine that has been proved to participate in diverse neurological diseases including seizures. Blockade of HMGB1 with neutralizing antibody has shown protective effects against different kinds of insults. However, the potential role of anti-HMGB1 antibody in status epilepticus (SE) has not yet been addressed. In the present study, we investigated the effects of anti-HMGB1 antibody on hippocampal damage and inflammatory reaction after SE induced by an intracerebroventricular kainic acid (KA) injection in postnatal day 21 rats. We found that KA-induced SE markedly increased the mRNA expression of interleukin-1β and tumor necrosis factor-α, microglial activation, and neuronal damage in the hippocampus. An intracerebroventricular injection of anti-HMGB1 antibody dose dependently inhibited the synthesis of cytokines, microglial activation, and neuronal losses in the hippocampus after SE. In conclusion, our findings suggest that HMGB1 blocking therapy exerts neuroprotective effects during the early phase of KA-induced SE in juvenile rats.