Effect of Taxifolin on Ethanol-Induced OxidativeBbrain Damage in Rats

ArticleAçık Erişim

Özet

Studies have shown that alcohol exerts the most severe toxic effect on central nervous system by increasing free oxygen radical production and suppressing endogenous antioxidant production. We aim to biochemically investigate the effect of taxifolin on ethanol-induced oxidative brain damage in rats. ( Sakarya Med J, 2018, 8(3):638-643 ). Materials and Methods Experimental animals were divided into healthy (SG), ethanol-receiving control (EtOH) and taxifolin+ethanol receiving (TEtOH) groups. At the end of the administration of ethanol and taxifolin, the animals were sacrifi ced by high dose anesthesia and brain tissues were removed. Malondialdehyde (MDA), lipid peroxidation product, and total glutathione (tGSH), endogenous antioxidant, levels in brain tissues were measured. Results MDA levels were signifi cantly higher in the rats in the EtOH group than in those in the TEtOH group (p<0.001). In contrast, tGSH levels were signifi cantly lower in the rats in the EtOH group than in those in the TEtOH group (p<0.001). Conclusion Our results suggest that taxifolin protects brain tissue from ethanol-induced oxidative damage.

Anahtar Kelimeler

RDL Kalıcı Bağlantı (PID)
https://rdlopen.rawdatalibrary.net/r/ebyu/20080Resmi atıflarda kullanılan kalıcı adres
Tam Kayıt
AlanDeğerDil
dc.contributor.authorBİLGİN, ASLI ÖZBEK
dc.contributor.authorSÜLEYMAN, BAHADIR
dc.contributor.authorMammadov, Renad
dc.date.accessioned2026-10-18T21:12:00.520514537Z
dc.date.available2026-10-18T21:12:00.520514537Z
dc.date.issued2018
dc.description.abstractStudies have shown that alcohol exerts the most severe toxic effect on central nervous system by increasing free oxygen radical production and suppressing endogenous antioxidant production. We aim to biochemically investigate the effect of taxifolin on ethanol-induced oxidative brain damage in rats. ( Sakarya Med J, 2018, 8(3):638-643 ). Materials and Methods Experimental animals were divided into healthy (SG), ethanol-receiving control (EtOH) and taxifolin+ethanol receiving (TEtOH) groups. At the end of the administration of ethanol and taxifolin, the animals were sacrifi ced by high dose anesthesia and brain tissues were removed. Malondialdehyde (MDA), lipid peroxidation product, and total glutathione (tGSH), endogenous antioxidant, levels in brain tissues were measured. Results MDA levels were signifi cantly higher in the rats in the EtOH group than in those in the TEtOH group (p<0.001). In contrast, tGSH levels were signifi cantly lower in the rats in the EtOH group than in those in the TEtOH group (p<0.001). Conclusion Our results suggest that taxifolin protects brain tissue from ethanol-induced oxidative damage.
dc.identifier.eissn2146-409X
dc.identifier.endpage643
dc.identifier.issue3
dc.identifier.startpage638
dc.identifier.urihttps://rdlopen.rawdatalibrary.net/r/ebyu/20080
dc.identifier.volume8
dc.language.isotr
dc.relation.ispartofSakarya Tıp Dergisi
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectTıbbi Araştırmalar Deneysel
dc.subjectKlinik Nöroloji
dc.subjectNörolojik Bilimler
dc.subjectFizyoloji
dc.subjectBiyokimya ve Moleküler Biyoloji
dc.titleEffect of Taxifolin on Ethanol-Induced OxidativeBbrain Damage in Rats
dc.typeArticle
dspace.entity.typePublication
rdl.citation.trdizin1
rdl.departmentERZİNCAN BİNALİ YILDIRIM ÜNİVERSİTESİ
rdl.source.indexTRDIZIN