Arabic Gum Could Alleviate the Aflatoxin B 1 -provoked Hepatic Injury in Rat: The Involvement of Oxidative Stress, Inflammatory, and Apoptotic Pathways.
Noha AhmedSamir Mohamed El RayesWaleed F KhalilAhmed AbdeenAfaf AbdelkaderMohammed YoussefZainab M MaherAmany N IbrahimShaymaa M AbdelrahmanSamah F IbrahimDoaa AbdelrahamanMohammed AlsieniOsama S ElserafyHeba I GhamryHanan T EmamObeid ShanabPublished in: Toxins (2022)
Aflatoxin B 1 (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 µg/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-α (TNF-α), interleukin (IL)-6, inducible nitric oxide synthase (iNOS), and nuclear factor kappa-B transcription factor/p65 (NF-κB/p65) mRNA expression levels. Interestingly, the antioxidant and anti-inflammatory contents of AG may reverse the induced oxidative damage, inflammation, and apoptosis in AF-exposed animals.
Keyphrases
- oxidative stress
- nuclear factor
- atrial fibrillation
- diabetic rats
- anti inflammatory
- cell death
- toll like receptor
- dna damage
- nitric oxide synthase
- induced apoptosis
- quantum dots
- transcription factor
- ischemia reperfusion injury
- nitric oxide
- high glucose
- healthcare
- endothelial cells
- rheumatoid arthritis
- highly efficient
- public health
- mental health
- drug induced
- cell cycle arrest
- hydrogen peroxide
- inflammatory response
- climate change
- working memory
- endoplasmic reticulum stress
- amyotrophic lateral sclerosis
- visible light
- heat stress
- dna binding