The protective role of ferulic acid on sepsis-induced oxidative damage in Wistar albino rats

Highlights • The effects of ferulic acid (FA) on sepsis-induced oxidative damage in thelymphocytes, liver and kidney cells of Wistar albino rats were investigated. • The DNA damage was found to be significantly higher in the sepsis-induced rats ( p < 0.05). • The Comet parameters were significant...

Ausführliche Beschreibung

Gespeichert in:

Bibliographische Detailangaben
Veröffentlicht in:	Environmental toxicology and pharmacology 2014-11, Vol.38 (3), p.774-782
Hauptverfasser:	Bacanlı, Merve, Aydın, Sevtap, Taner, Gökçe, Göktaş, Hatice Gül, Şahin, Tolga, Başaran, A. Ahmet, Başaran, Nurşen
Format:	Artikel
Sprache:	eng
Schlagworte:	Alkaline single cell electrophoresis Animals Antioxidants - administration & dosage Antioxidants - pharmacology Coumaric Acids - administration & dosage Coumaric Acids - pharmacology DNA damage DNA Damage - drug effects Emergency Ferulic acid Gene Expression Regulation - drug effects Glutathione - metabolism Glutathione Peroxidase - metabolism Kidney - metabolism Liver - metabolism Lymphocytes - metabolism Malondialdehyde - metabolism Oxidative Stress - drug effects Rats Rats, Wistar Sepsis Sepsis - metabolism Sepsis - pathology Superoxide Dismutase - metabolism
Online-Zugang:	Volltext
Tags:	Tag hinzufügen Keine Tags, Fügen Sie den ersten Tag hinzu!

Beschreibung
Zusammenfassung:	Highlights • The effects of ferulic acid (FA) on sepsis-induced oxidative damage in thelymphocytes, liver and kidney cells of Wistar albino rats were investigated. • The DNA damage was found to be significantly higher in the sepsis-induced rats ( p < 0.05). • The Comet parameters were significantly decreased in the FA-treated sepsis-induced group when compared with the sepsis-induced group. • FA treatment also decreased the malondialdehyde (MDA) levels and glutathione peroxidase (GSH-Px) activities and increased the glutathione (GSH) levels and superoxide dismutase (SOD) activities in the sepsis-induced rats.
ISSN:	1382-6689 1872-7077
DOI:	10.1016/j.etap.2014.08.018