Relationship Between Oxidative Stress, Tau Level and Antioxidant Mechanisms of the KEAP-1/NRF-2/HO-1 in Children with Hydrocephalus

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dc.authorscopusid57201446607
dc.authorscopusid57203094952
dc.authorscopusid55798385900
dc.authorscopusid6505572991
dc.authorscopusid56928021200
dc.contributor.authorGuzelcicek, Ahmet
dc.contributor.authorKoyuncu, Ismail
dc.contributor.authorGönel, Ataman
dc.contributor.authorCigdem, Gulyara
dc.contributor.authorKaradag, Mehmet
dc.date.accessioned2024-09-19T15:48:34Z
dc.date.available2024-09-19T15:48:34Z
dc.date.issued2021
dc.departmentHatay Mustafa Kemal Üniversitesien_US
dc.description.abstractBackground: Hydrocephalus is a complex neurologic disorder that has a widespread impact on the central nervous system and a multifactor disease which affects the CSF dynamics and causes severe neurological impairments in children. The pathophysiology of hydrocephalus is not fully understood. However, increasing evidence suggests that oxidative stress may be an important factor in the pathogenesis of hydrocephalus. Objective: The purpose of this study is to investigate the relationship of the KEAP-1/NRF-2/HO-1 pathway, one of the main regulators of the antioxidant system in the hydrocephalus pathology, on oxidative stress and tau protein level. Methods: The study included 32 patients with hydrocephalus and 32 healthy controls. KEAP-1, NRF-2, HO-1, TAU, and MPO levels are measured using ELISA method TAS, TOS, and Total THIOL colorimetric method. Results: KEAP-1, TAS, and Total THIOL levels were found significantly lowerer in the hydrocephalus group than in the control group. Nevertheless, it was identified that in the hydrocephalus group that the NRF-2, HO-1, TAU, MPO, TOS, and OSI levels were significantly elevated. Conclusion: In conclusion, although the KEAP-1/NRF-2/HO-1 pathway is activated in patients with hydrocephalus, it is identified that the antioxidant defense system is insufficient and ultimately leads to elevated oxidative stress. The elevation in the tau level may be an indicator of oxidative stress induced neurodegenerative damage. © 2021 Bentham Science Publishers.en_US
dc.identifier.doi10.2174/1871523019666201228111713
dc.identifier.endpage289en_US
dc.identifier.issn1871-5230
dc.identifier.issue3en_US
dc.identifier.pmid33371862en_US
dc.identifier.scopus2-s2.0-85122165971en_US
dc.identifier.scopusqualityQ3en_US
dc.identifier.startpage282en_US
dc.identifier.urihttps://doi.org/10.2174/1871523019666201228111713
dc.identifier.urihttps://hdl.handle.net/20.500.12483/15159
dc.identifier.volume20en_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherBentham Science Publishersen_US
dc.relation.ispartofAnti-Inflammatory and Anti-Allergy Agents in Medicinal Chemistryen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectHO-1en_US
dc.subjectHydrocephalusen_US
dc.subjectKEAP-1en_US
dc.subjectNRF-2en_US
dc.subjectOxidative stressen_US
dc.subjectTAUen_US
dc.titleRelationship Between Oxidative Stress, Tau Level and Antioxidant Mechanisms of the KEAP-1/NRF-2/HO-1 in Children with Hydrocephalusen_US
dc.typeArticleen_US

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