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

Abstract

Background: 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.

Objectives: The study aimed 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-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.

Conclusion: The results indicating that Magnolia officinalis is an alternative preventive treatment for early stages of epileptogenesis are encouraging.

Keywords: Kainic acid; Magnolia officinalis; Status epilepticus; epileptogenesis; neuroinflammation; neuroprotection..