Na,K-ATPase Activity in the Hippocampus of the Pilocarpine-Induced Rat Model of Epilepsy Treated with Benzylidene Digoxin 15 (BD15)

Na,K-ATPase Activity in the Hippocampus of the Pilocarpine-Induced Rat Model of Epilepsy Treated with Benzylidene Digoxin 15 (BD15)

• Author
• Ítalo Leonardo Diogo
• Co-authors
• Felipe Santos Teixeira , Julia Lopes Granato , Gabriella Rodrigues Barbosa , Matheus Vieira Machado , Israel José Pereira Garcia , Hérica de Lima Santos , Vanessa Faria Cortes , José Augusto Ferreira Perez Villar , Leandro Augusto Barbosa , Cristiane Queixa Tilelli , Luciana Estefani Drumond de Carvalho
• Abstract

• Na,K-ATPase (NKA) is an essential enzyme in maintaining the sodium and potassium ion gradient across the plasma membrane of neuronal cells, playing a crucial role in regulating neuronal excitability and ionic homeostasis. Dysfunctions in NKA have been associated with various neurological conditions, including epilepsy. Studies indicate that genetic mutations affecting NKA functionality can lead to imbalances in ion concentrations, resulting in neuronal hyperexcitability and a predisposition to epileptic seizures. Thus, NKA emerges as a key point in understanding the underlying pathophysiological mechanisms of epilepsy and a potential therapeutic target for developing new treatments. Semi-synthetic analogue to digoxin, benzylidene digoxin 15 (BD15), has shown promise as a neuroprotective drug. Therefore, this study aims to evaluate the effect of BD-15 on NKA activity in an experimental model of temporal lobe epilepsy. Male Wistar rats were induced with pilocarpine (300 mg/kg; i.p.) and assessed for status epilepticus (SE). The animals were then divided into groups: CTR (control); CTR+BD15 (control with BD15); NSE (no SE); NSE+BD15 (no SE with BD15); SE (with SE) and SE+BD15 (with SE with BD15). The animals received BD15 (100 µg/kg; i.p.) for 3 days, while the others received 0.9% saline. On the seventh day, the animals were euthanized, and the hippocampus was collected. A homogenate was prepared from the sample, and the total NKA activity, as well as the activities of the alpha 1, 2, and 3 isoforms, were measured. The results show that the NSE and SE groups had reduced total activity and reduced activities of the alpha 2 and 3 isoforms, while the groups treated with BD15 had values similar to the control group. No difference was observed in the activity of alpha 1 among the groups. Thus, we observed that the experimental model of Temporal Lobe Epilepsy showed a normalization of NKA activity with BD15 treatment.

• Keywords
• Epilesy, BD-15, Na Pump, Neuroprotection, Hippocampus
• Subject Area
• Na Pump

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