Magnolia officinalis Reduces Inflammation and Damage Induced by Recurrent Status Epilepticus in Immature Rats.

Abstract

Neuroinflammation induced in response to damage caused by status epilepticus (SE) activates the interleukin (IL)1-β pathway and proinflammatory proteins that increase vulnerability to the development of spontaneous seizure activity and/or epilepsy. The study aimed to assess the short-term anti-inflammatory and neuroprotective effects of Magnolia officinalis (MO) on recurrent SE in immature rats. Sprague-Dawley rats at PN day 10 were used; n = 60 rats were divided into two control groups, SHAM and KA, and two experimental groups, MO (KA-MO) and Celecoxib (KA-Clbx). The anti-inflammatory effect of a single dose of MO was evaluated at 6 and 24 hr by Western blotting and on day 30 PN via a subchronic administration of MO to assess neuronal preservation and hippocampal gliosis by immunohistochemistry for NeunN and GFAP, respectively. KA-MO caused a decrease in the expression of IL1-β and Cox-2 at 6 and 24 h post-treatment, a reduction in iNOS synthase at 6 and 24 hr post-treatment and reduced neuronal loss and gliosis at postnatal day 30, similar to Clbx. The results indicating that Magnolia officinalis is an alternative preventive treatment for early stages of epileptogenesis are encouraging.