作者: Aziza Alrafiah , Hala Eweis , Hadeel Alsaegh , Fatemah Kamal
DOI: 10.3390/PH14040380
关键词: Glutathione 、 Pilocarpine 、 Oxidative stress 、 HMGB1 、 Celecoxib 、 Inflammation 、 Pharmacology 、 Medicine 、 Epilepsy 、 Valproic Acid
摘要: The risk of developing epilepsy is strongly linked to peripheral inflammatory disorders in humans. High-mobility group box protein 1 (HMGB1) has the most focus for being a suspect this scenario. current study aimed detect celecoxib effect, an anti-inflammatory drug, on decreasing seizure susceptibility and organ damage lipopolysaccharides (LPS)/pilocarpine (PILO) pretreated Wistar rats. Rats were divided into 6 groups (8 each): (control), 2 (PILO), 3 (PILO+LPS), 4 (PILO+LPS+(VPA) Valproic acid), 5 (PILO+LPS+Celecoxib), (PILO+LPS+VPA+Celecoxib). LPS was used induce sepsis PILO seizures. Oxidative stress markers, pro-inflammatory cytokines, HMGB1 levels serum brain homogenate evaluated. Histopathological studies conducted hippocampus, liver, lung, kidney. Treatment with either alone or combination VPA significantly reduced Racine score delays latency generalized tonic-clonic seizures onset significant decrease hippocampal oxidative increase glutathione. In addition, treatment suppressed HMGB1translocation circulation more than alone. Furthermore, kidney histopathological changes improved contrast other epileptic groups. Celecoxib combined antiepileptic multiorgan protective effects acute models induced by LPS. It decreased findings, oxidative, This might be due its anti-oxidative, anti-HMGB1 mediated effects.