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Sinapic acid reduces pentylenetetrazol induced seizures in rats

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Title Sinapic acid reduces pentylenetetrazol induced seizures in rats
 
Creator Ekici, Mehmet
Güneş, Handan
Gezer, Arzu
 
Subject Anticonvulsant activity
Antiseizure activity
Apoptosis
Brain-derived neurotrophic factor (BDNF)
Epilepsy
Experimental acute seizure model
Generalized tonic-clonic seizures (GTCS)
Inflammation
Oxidative stress
Racine convulsion scale (RCS)
 
Description 379-392
Seizure is known to induce oxidative stress which may initiate neuronal death. Oxidant-antioxidant imbalance often leads
to mitochondrial dysfunction, inflammation, and apoptosis in the brain which may further result in the development of
seizure. Phenolic compounds such as curcumin and rosmarinic acid are reported to control convulsions and seizures in
pentylenetetrazol induced seizures models by suppressing seizure time, oxidative stress and inflammation indirectly. Sinapic
acid (SA), a polyphenolic product of hydroxycinnamic acid found in various plants, exhibits anti-inflammatory, antioxidant
and anxiolytic effects. In this study, we investigated the effects of sinapic acid on pentylenetetrazol induced seizures in rats
through oxidative stress, inflammation, apoptosis, and neurotrophic factor. A total of 28 male Wistar Albino rats weighing
200-220 g were divided into four equal groups (n=7/group). The treatment groups received 10 mg/kg and 20 mg/kg SA,
respectively, by oral gavage for five consecutive days along with pentylenetetrazol (45 mg/kg, intraperitoneal) to induce
seizures. The levels of Total oxidant status (TOS), Total antioxidant status (TAS), TNF-α, IL-1β, and Brain-derived
neurotrophic factor (BDNF) were measured in the cortex and hippocampus. Additionally, caspase 3 and caspase 9 levels, as
well as the immunoreactivity of Cleaved caspase 3, were determined in the hippocampus. The results showed that
pretreatment with 20 mg/kg SA delayed the latency of generalized tonic-clonic seizures (GTCS) and first myoclonic jerk,
reduced GTCS duration, and improved seizure score and cognitive function. Importantly, the 20 mg/kg SA pretreatment
resulted in decreased levels of TOS, TNF-α, IL-1β, and BDNF in the cortex and hippocampus, while increasing TAS levels
in these brain areas. Moreover, the 20 mg/kg SA reduced hippocampal caspase 3 and caspase 9 levels, as well as the
immunoreactivity of Cleaved caspase 3 in rats with pentylenetetrazol-induced seizures. These findings suggest that the
anti-seizure effects of SA are mediated by BDNF modulation, as well as its antioxidant, anti-inflammatory, and antiapoptotic
properties.
 
Date 2024-05-31T09:38:12Z
2024-05-31T09:38:12Z
2024-06
 
Type Article
 
Identifier 0975-1009 (Online); 0019-5189 (Print)
http://nopr.niscpr.res.in/handle/123456789/64017
https://doi.org/10.56042/ijeb.v62i06.4177
 
Language en
 
Publisher NIScPR-CSIR,India
 
Source IJEB Vol.62(06) [June 2024]