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...

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Published inEnvironmental toxicology and pharmacology Vol. 38; no. 3; pp. 774 - 782
Main Authors Bacanlı, Merve, Aydın, Sevtap, Taner, Gökçe, Göktaş, Hatice Gül, Şahin, Tolga, Başaran, A. Ahmet, Başaran, Nurşen
Format Journal Article
LanguageEnglish
Published Netherlands Elsevier B.V 01.11.2014
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Abstract 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.
AbstractList Oxidative stress has an important role in the development of sepsis-induced multiorgan failure. Ferulic acid (FA), a well-established natural antioxidant, has several pharmacological activities including anti-inflammatory, anticancer and hepatoprotective. This study aimed to investigate the effects of FA on sepsis-induced oxidative damage in Wistar albino rats. Sepsis-induced DNA damage in the lymphocytes, liver and kidney cells of rats were evaluated by comet assay with and without formamidopyrimidine DNA glycosylase (Fpg). The oxidative stress parameters such as superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities and total glutathione (GSH) and malondialdehyde (MDA) levels were also measured. It is found that DNA damage in sepsis+FA-treated group was significantly lower than the sepsis group. FA treatment also decreased the MDA levels and increased the GSH levels and SOD and GSH-Px activities in the sepsis-induced rats. It seems that FA might have ameliorative effects against sepsis-induced oxidative damage.
•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. Oxidative stress has an important role in the development of sepsis-induced multiorgan failure. Ferulic acid (FA), a well-established natural antioxidant, has several pharmacological activities including anti-inflammatory, anticancer and hepatoprotective. This study aimed to investigate the effects of FA on sepsis-induced oxidative damage in Wistar albino rats. Sepsis-induced DNA damage in the lymphocytes, liver and kidney cells of rats were evaluated by comet assay with and without formamidopyrimidine DNA glycosylase (Fpg). The oxidative stress parameters such as superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities and total glutathione (GSH) and malondialdehyde (MDA) levels were also measured. It is found that DNA damage in sepsis+FA-treated group was significantly lower than the sepsis group. FA treatment also decreased the MDA levels and increased the GSH levels and SOD and GSH-Px activities in the sepsis-induced rats. It seems that FA might have ameliorative effects against sepsis-induced oxidative damage.
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.
Author Aydın, Sevtap
Başaran, A. Ahmet
Bacanlı, Merve
Taner, Gökçe
Şahin, Tolga
Başaran, Nurşen
Göktaş, Hatice Gül
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/25305738$$D View this record in MEDLINE/PubMed
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Issue 3
Keywords Sepsis
DNA damage
Alkaline single cell electrophoresis
Ferulic acid
Language English
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Snippet Highlights • The effects of ferulic acid (FA) on sepsis-induced oxidative damage in thelymphocytes, liver and kidney cells of Wistar albino rats were...
•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...
Oxidative stress has an important role in the development of sepsis-induced multiorgan failure. Ferulic acid (FA), a well-established natural antioxidant, has...
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SubjectTerms 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
Title The protective role of ferulic acid on sepsis-induced oxidative damage in Wistar albino rats
URI https://www.clinicalkey.es/playcontent/1-s2.0-S138266891400204X
https://dx.doi.org/10.1016/j.etap.2014.08.018
https://www.ncbi.nlm.nih.gov/pubmed/25305738
https://search.proquest.com/docview/1629973713
https://search.proquest.com/docview/1746891363
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