Gallic acid mitigates diclofenac-induced liver toxicity by modulating oxidative stress and suppressing IL-1β gene expression in male rats.
Mohsen EsmaeilzadehEsfandiar HeidarianMehrnoosh ShaghaghiHoshang RoshanmehrMohammad NajafiAlireza MoradiAli NouriPublished in: Pharmaceutical biology (2021)
The data demonstrated that the liver levels of the GSH, GPx, SOD, and CAT significantly reduced and the levels of the serum protein carbonyl, AST, ALP, ALT, total bilirubin, MDA, serum IL-1β, and the liver IL-1β gene expression were remarkably increased in the second group compared to control group. On the other hand, treatment with GA led to a significant elevation in GSH, GPx, SOD, CAT, and a significant decrease in protein carbonyl, AST, ALP, ALT, total bilirubin, MDA, serum IL-1β, and gene expression of IL-1β in comparison with the second group. Histological changes were also ameliorated by GA oral administration. Discussion and Conclusions: The data show that the oral administration of GA could alleviate the noxious effects of DIC on the antioxidant defense system and liver tissue.
Keyphrases
- gene expression
- oxidative stress
- pet ct
- dna methylation
- diabetic rats
- electronic health record
- amino acid
- breast cancer cells
- big data
- dna damage
- drug induced
- high glucose
- cell proliferation
- cell death
- endoplasmic reticulum stress
- induced apoptosis
- combination therapy
- anti inflammatory
- endothelial cells
- replacement therapy
- data analysis
- heat stress