title: Effect of galangin supplementation on oxidative damage and inflammatory changes in fructose-fed rat liver.
abstract: The study examined the effects of galangin (GA) on oxidative stress, inflammatory cytokine levels and nuclear factor-kappa B (NF-κB) activation in fructose-fed rat liver. Adult male albino Wistar rats were divided into 4 groups. Groups 1 and 4 received the control diet containing starch as the source of carbohydrate while groups 2 and 3 were fed a diet containing fructose. Groups 3 and 4 additionally received GA (100μg/kg, p.o) from the 15th day. At the end of 60 days, the levels of plasma glucose, insulin and triglycerides, insulin sensitivity indices and oxidative stress markers in the liver were determined. Cytokines of interest were assayed by ELISA and RT-PCR and NF-κB p65 nuclear translocation by Western blot and RT-PCR. Compared to control diet-fed animals, fructose-fed animals developed hyperglycemia, hyperinsulinemia, hypertriglyceridemia and insulin resistance (IR) (all p<0.01). GA prevented the rise in plasma glucose, insulin and triglycerides and improved insulin sensitivity. Tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) levels in plasma and the mRNA and protein levels of TNF-α and transforming growth factor-β1(TGF-β(1)) in liver were significantly higher in fructose-fed rats than control rats. However, treatment with GA downregulated the expression of these cytokines. Translocation of NF-κB into the nucleus was also increased in fructose diet-fed animals, which was prevented by GA. These results suggest that GA prevents oxidative damage and has a downregulatory effect on the inflammatory pathway in liver of fructose-fed rats.
authors.affiliation: Department of Biochemistry and Biotechnology, Annamalai University, Annamalainagar, Tamil Nadu, India.
authors.forename: Allur Subramaniyan
authors.initials: AS
authors.lastname: Sivakumar
authors.forename: Carani Venkatraman
authors.initials: CV
authors.lastname: Anuradha
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000378:metabolism; D001786:Blood Glucose / Q000187:drug effects / Q000378:metabolism; D001835:Body Weight / Q000187:drug effects; D002467:Cell Nucleus / Q000378:metabolism; D056486:Chemical and Drug Induced Liver Injury / Q000097:blood / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D003094:Collagen / Q000378:metabolism; D003600:Cytosol / Q000378:metabolism; D004040:Dietary Carbohydrates / Q000008:administration & dosage / Q000494:pharmacology*; D019587:Dietary Supplements; D005419:Flavonoids / Q000008:administration & dosage / Q000494:pharmacology* / Q000627:therapeutic use; D016166:Free Radical Scavengers / Q000008:administration & dosage / Q000494:pharmacology; D005632:Fructose / Q000008:administration & dosage / Q000494:pharmacology*; D015870:Gene Expression / Q000187:drug effects / Q000235:genetics; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance / Q000502:physiology; D015850:Interleukin-6 / Q000097:blood; D008054:Lipid Peroxides / Q000097:blood; D008099:Liver / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D008297:Male; D018384:Oxidative Stress / Q000187:drug effects*; D050050:Protein Carbonylation / Q000187:drug effects; D051381:Rats; D017208:Rats, Wistar; D051996:Transcription Factor RelA / Q000235:genetics / Q000378:metabolism; D053773:Transforming Growth Factor beta1 / Q000235:genetics; D014280:Triglycerides / Q000097:blood; D014409:Tumor Necrosis Factor-alpha / Q000097:blood / Q000235:genetics
chemical_list: D000975:Antioxidants; D001786:Blood Glucose; D004040:Dietary Carbohydrates; D005419:Flavonoids; D016166:Free Radical Scavengers; D007328:Insulin; D015850:Interleukin-6; D008054:Lipid Peroxides; D051996:Transcription Factor RelA; D053773:Transforming Growth Factor beta1; D014280:Triglycerides; D014409:Tumor Necrosis Factor-alpha; C037032:galangin; D005632:Fructose; D003094:Collagen