Astrocytes, the most abundant glial cells, have several metabolic functions, including ionic,
neurotransmitter and energetic homeostasis for neuronal activity. Reactive astrocytes and their dysfunction have been associated with several
brain disorders, including the epileptogenic process.
Glial Fibrillary Acidic Protein (GFAP) and S100
calcium-binding protein B (S100B) are astrocyte
biomarkers associated with
brain injury. We hypothesize that
arundic acid (ONO-2506), which is known as an inhibitor of S100B synthesis and secretion, protects the hippocampal tissue from
neuroinflammation and astrocyte dysfunction after status epileptics (SE) induction by Li-
pilocarpine in young rats. Herein, we investigated the effects of
arundic acid treatment, at time points of 6 or 24 h after the induction of SE by Li-
pilocarpine, in young rats. In SE animals,
arundic acid was able to prevent the damage induced by Li-
pilocarpine in the hippocampus, decreasing neuroinflammatory signaling (reducing IL-1β, COX2, TLR4 and RAGE contents),
astrogliosis (decreasing GFAP and S100B) and astrocytic dysfunction (recovering levels of GSH,
glutamine synthetase and
connexin-43). Furthermore,
arundic acid improved
glucose metabolism and reduced the
glutamate excitotoxicity found in
epilepsy. Our data reinforce the role of astrocytes in epileptogenesis development and the neuroprotective role of
arundic acid, which modulates astrocyte function and
neuroinflammation in SE animals.