2018
DOI: 10.5530/ijper.52.1.4
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Curcumin: The Molecular Mechanisms of Action in Inflammation and Cell Death during Kainate-Induced Epileptogenesis

Abstract: Background: Recent preclinical studies demonstrated the potential antiepileptogenic effect of curcumin. Its molecular pathways in modulating epileptogenesis remain unclear. Objectives: This study investigated the epileptogenic processes induced by kainic acid (KA) and to investigate the antiepileptogenic pathways associated with curcumin therapy. Methods: A single dose of KA 10 mg/kg was used to induce a convulsive status epilepticus in female Wistar rats. After one week of curcumin treatment, gene expression … Show more

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Cited by 8 publications
(2 citation statements)
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“…Even so, the exact mechanisms through which the anti-inflammatory properties of C. longa are implemented are still unknown, although some authors have reported that it upregulates genes related to the anti-inflammatory cytokines and reduces the expression of pro-inflammatory cytokines, such as IL-1β and TNF-α ( Hashemian et al, 2017 ; Yin et al, 2018 ). One other potential mechanism, described by Peng et al (2021) , is the inhibition of the expression of the iNOS gene by C. longa that interferes with the nitric oxide synthase pathway.…”
Section: Discussionmentioning
confidence: 99%
“…Even so, the exact mechanisms through which the anti-inflammatory properties of C. longa are implemented are still unknown, although some authors have reported that it upregulates genes related to the anti-inflammatory cytokines and reduces the expression of pro-inflammatory cytokines, such as IL-1β and TNF-α ( Hashemian et al, 2017 ; Yin et al, 2018 ). One other potential mechanism, described by Peng et al (2021) , is the inhibition of the expression of the iNOS gene by C. longa that interferes with the nitric oxide synthase pathway.…”
Section: Discussionmentioning
confidence: 99%
“…The harmful effects, which are toxic to tissues, occur primarily through the production of free radicals [12,13]. This reaction is important in removing damaged cells from the brain tissue; however, it can also increase the harm to brain cells by producing free radicals that are toxic to healthy cells [2,14,15]. There has been an increasing amount of evidence suggesting that ischemic inflammation may be vital to the issue of pathogens, as ischemic stroke results not only in damage and neuronal loss but also in sustained neuroinflammation after stroke [3,16,17].…”
Section: Introductionmentioning
confidence: 99%