ABSTRACT
BACKGROUND: Epilepsy is one of the major neurological disorders. The inflammatory process and oxidative stress are closely related to seizure progression. Quercetin is a flavonoid with anti-inflammatory and antioxidant properties as well as neuroprotective effects. We aimed to evaluate the effect of quercetin on pentylenetetrazole- (PTZ-) induced seizures in male mice focusing on its possible anti-neuroinflammatory and anti-oxidative stress. METHODS: In this study, 50 male NMRI mice were divided into five groups (n = 10) and given the following treatments: normal saline, quercetin at doses of 10, 20, and 40 mg/kg, and diazepam at a dose of 10 mg/kg. In order to induce seizures, PTZ was administered intravenously. Drugs were administered intravenously 60 min before the seizure induction. The seizure threshold was measured, and finally, malondialdehyde (MDA), total antioxidant capacity (TAC), and the gene expression of IL-1ß, TNF-α, NLRP3, and iNOS were determined in the prefrontal cortex. RESULTS: It was confirmed that quercetin increased the seizure threshold. And quercetin increased TAC, and decreased levels of MDA as well as gene expression of TNF- α, NLRP3, IL-1ß, and iNOS in the prefrontal cortex at the time of seizure induction. CONCLUSION: It was suggested that the anticonvulsant effect of quercetin in PTZ-induced seizures in mice may be due to the reduction of inflammatory responses and oxidative stress in the prefrontal cortex.
Subject(s)
Anticonvulsants , Pentylenetetrazole , Mice , Male , Animals , Anticonvulsants/therapeutic use , Quercetin/pharmacology , Antioxidants/pharmacology , NLR Family, Pyrin Domain-Containing 3 Protein/metabolism , Seizures/chemically induced , Seizures/drug therapy , Seizures/metabolism , Oxidative Stress , Mice, Inbred Strains , Tumor Necrosis Factor-alpha/metabolism , Disease Models, AnimalABSTRACT
Free radical-induced neural damage is implicated in cerebral hypoperfusion disorders and antioxidants have protective effects. In the present study, we examined the effect of gallic acid (GA; 100mg/kg, p.o. for 10 days) on cognitive deficit and cerebral oxidative stress induced by permanent bilateral common carotid artery occlusion (2VO) as an animal model of vascular dementia (VD). The results showed that 2VO significantly reduced the spatial memory performance in Morris water maze as well as non-enzymatic (total thiol) and enzymatic [glutathione peroxidase (GPx)] antioxidant contents and increased the level of malondialdehyde (MDA) in the hippocampus and frontal cortex of vehicle-treated group as compared to sham-operated rats. Furthermore, chronic administration of GA significantly restored the spatial memory, total thiol and GPx contents and also decreased MDA levels in these tissues. GA alone did not show any change neither in the status of various antioxidants nor behavioral tests over sham values. The results demonstrate that GA has beneficial activity against 2VO-induced cognitive deficits via enhancement of cerebral antioxidant defense. Taken together, the present study suggested that GA might be useful in the treatment of VD.
