Aflatoxin B1 (AF) is an unavoidable environmental pollutant that contaminates food,
feed, and grains, which seriously threatens human and animal health. Arabic gum (AG) has recently
evoked much attention owing to its promising therapeutic potential. Thus, the current
study was conducted to look into the possible mechanisms beyond the ameliorative activity of AG
against AF-inflicted hepatic injury. Male Wistar rats were assigned into four groups: Control, AG
(7.5 g/kg b.w/day, orally), AF (200 g/kg b.w), and AG plus AF group. AF induced marked liver
damage expounded by considerable changes in biochemical profile and histological architecture.
The oxidative stress stimulated by AF boosted the production of plasma malondialdehyde (MDA)
level along with decreases in the total antioxidant capacity (TAC) level and glutathione peroxidase
(GPx) activity. Additionally, AF exposure was associated with down-regulation of the nuclear factor
erythroid2–related factor2 (Nrf2) and superoxide dismutase1 (SOD1) protein expression in liver
tissue. Apoptotic cascade has also been evoked following AF-exposure, as depicted in overexpression
of cytochrome c (Cyto c), cleaved Caspase3 (Cl. Casp3), along with enhanced up-regulation of
inflammatory mediators such as tumor necrosis factor- (TNF- ), interleukin (IL)-6, inducible nitric
oxide synthase (iNOS), and nuclear factor kappa-B transcription factor/p65 (NF-B/p65) mRNA |
