Magnolia Officinalis Reduces Inflammation And Damage Induced By Recurrent Status Epilepticus In Immature Rats

BACKGROUND: Neuroinflammation induced in response to damage caused by status epilepticus (SE) activates the interleukin (IL)1-beta pathway and proinflammatory proteins that increase vulnerability to the development of spontaneous seizure activity and/or epilepsy. OBJECTIVES: To assess the short-term anti-inflammatory and neuroprotective effects of Magnolia officinalis (MO) on recurrent SE in immature rats. METHODS: 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. RESULTS: KA-MO caused a decrease in the expression of IL1-beta 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. CONCLUSION: The results indicating that Magnolia officinalis is an alternative preventive treatment for early stages of epileptogenesis are encouraging.