Ferulic Acid Attenuates Kainate-induced Neurodegeneration in a Rat Poststatus Epilepticus Model.

Autor:	Suha AJ; Department of Physiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.; Electrophysiology Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran., Sadr SS; Department of Physiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.; Electrophysiology Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran., Roghani M; Neurophysiology Research Center, Shahed University, Tehran, Iran., Haftcheshmeh SM; Department of Basic Medical Sciences, Neyshabur University of Medical Sciences, Neyshabur, Iran.; Healthy Ageing Research Centre, Neyshabur University of Medical Sciences, Neyshabur, Iran., Khamse S; Department of Physiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.; Electrophysiology Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran., Momtazi-Borojeni AA; Department of Medical Biotechnology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.; Iran's National Elites Foundation, Tehran, Iran.
Jazyk:	angličtina
Zdroj:	Current molecular pharmacology [Curr Mol Pharmacol] 2023; Vol. 16 (2), pp. 178-187.
DOI:	10.2174/1874467215666220225093737
Abstrakt:	Background and Aims: Increasing research evidence indicates that temporal lobe epilepsy (TLE) induced by kainic acid (KA) has high pathological similarities with human TLE. KA induces excitotoxicity (especially in the acute phase of the disease), which leads to neurodegeneration and epileptogenesis through oxidative stress and inflammation. Ferulic acid (FA) is one of the well-known phytochemical compounds that have shown potential antioxidant and anti-inflammatory properties and promise in treating several diseases. The current study set out to investigate the neuroprotective effects of FA in a rat model of TLE. Methods: Thirty-six male Wistar rats were divided into four groups. Pretreatment with FA (100 mg/kg/day p.o.) started one week before the intrahippocampal injection of KA (0.8 μg/μl, 5μl). Seizures were recorded and evaluated according to Racine's scale. Oxidative stress was assessed by measuring its indicators, including malondialdehyde (MDA), nitrite, and catalase. Histopathological evaluations including Nissl staining and immunohistochemical staining of cyclooxygenase-2 (COX-2), and neural nitric oxide synthases (nNOS) were performed for the CA3 region of the hippocampus. Results: Pretreatment with FA significantly attenuates the severity of the seizure and prevents neuronal loss in the CA3 region of the hippocampus in rats with KA-induced post-status epilepticus. Also, nitrite concentration and nNOS levels were markedly diminished in FA-pretreated animals compared to non-pretreated epileptic rats. Conclusion: Our findings indicated that neuroprotective properties of FA, therefore, could be considered a valuable therapeutic supplement in treating TLE. (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)
Databáze:	MEDLINE
Externí odkaz:	Zobrazit plný text záznamu