Genistein protects epilepsy-induced brain injury through regulating the JAK2/STAT3 and Keap1/Nrf2 signaling pathways in the developing rats.

Background: Epilepsy is a common chronic neurological disease. Recurrent seizures can cause irreversible brain damage. This study aimed to explore the regulation of Genistein on JAK2/STAT3 and Keap1/Nrf2 signaling pathway and the protective effects on brain injury after epilepsy.

Everolimus inhibits PI3K/Akt/mTOR and NF-kB/IL-6 signaling and protects seizure-induced brain injury in rats.

Background: Epilepsy is a common chronic neurological disease caused by the over-synchronization of neurons leading to brain dysfunction. Recurrent seizures can lead to cognitive and behavioral deficits, and irreversible brain damage. While the PI3K/Akt/mTOR pathway regulates various physiological processes of neurons and glia, it may also lead to abnormal neuronal signal transduction under pathological conditions, including that of epilepsy.

[Regulatory mechanism of MS275 on the p38 MAPK signaling pathway in rats with convulsion in the developmental stage].

Objective: To study the regulatory mechanism of MS275, a histone deacetylase inhibitor, on the p38 MAPK signaling pathway in rats with convulsion in the developmental stage.

Methods: Thirty-two male rats were randomly divided into four groups: control, pentylenetetrazol (PTZ), PTZ+3 mg/kg MS275, and PTZ+6 mg/kg MS275 (n=8 each). A rat model of convulsion in the developmental stage was prepared by an intraperitoneal injection of PTZ.

MS275 reduces seizure-induced brain damage in developing rats by regulating p38 MAPK signaling pathways and epigenetic modification.

Seizure is a common acute and severe disease in infants and children. Recurrent seizures or persistent seizures may cause irreversible brain damage. Mitogen activated protein kinase (MAPK) signaling pathway is associated with an inflammatory response, however it's involvement in the pathological process of seizures is not clear.

Histone deacetylase inhibitor SAHA attenuates post-seizure hippocampal microglia TLR4/MYD88 signaling and inhibits TLR4 gene expression via histone acetylation.

Background: Epilepsy is a common neurological disorder characterized by recurrent unprovoked seizures. Seizure-induced TLR4/MYD88 signaling plays a critical role in activating microglia and triggering neuron apoptosis. SAHA is a histone deacetylase inhibitor that regulates gene expression by increasing chromatin histone acetylation.