Abstract

Aim: Valproic acid (VPA) is a commonly used antiepileptic drug and known to have a neurotoxic effect, but its mechanism is not yet understood. In the present study, we aimed to determine how the VPA causes cell death in the brain and to evaluate the protective effects of thymoquinone (TQ) on VPA-induced brain damage.
Materials and Methods: Male Sprague–Dawley albino rats were divided into three groups: control, VPA (500 mg/kg/day) and VPA + TQ (500 mg/kg/day + 50 mg/kg/day) with seven rats in. At the end of the experiment, rats were sacrificed and brain samples were taken to measure the expression levels of Receptor-interacting serine/threonine-protein kinase-1 (RIPK1) and -3 (RIPK3) genes by quantitative real-time PCR (qRT-PCR), NADPH oxidase-4 (NOX4) and, caspase-3 (CAS-3) expression by immunohistochemistry and the structural changes in the brain tissue by histologically.
Results: RIPK1 gene expression levels were significantly increased in the VPA group compared to the controls (p

Key words: Apoptosis; RIPK1; thymoquinone; valproic acid