1
2
3
4
5
6
7
8
9
10
*Corresponding Author: Jing Zhao,
Aflatoxin B1 (AFB1), a hepatotoxic mycotoxin produced by Aspergillus species, poses significant health risks through food contamination. Piperine, the bioactive alkaloid from black pepper, exhibits diverse pharmacological properties including hepatoprotection.
Forty male Wistar rats were divided into four groups (n = 10): control (saline), AFB1 (100 μg/kg/day), piperine (1.12 mg/kg/day) and a combination group receiving piperine (1.12 mg/kg/day) one hour before AFB1 (100 μg/kg/day) for 28 days. Treatments were administered intraperitoneally for 28 days. Liver function tests, oxidative stress markers, inflammatory cytokines, apoptotic proteins and histopathological changes were evaluated.
AFB1 exposure significantly elevated liver enzymes (aspartate aminotransferase [AST], alanine aminotransferase [ALT], alkaline phosphatase [ALP]) and decreased albumin levels. Oxidative stress was evident through increased malondialdehyde (MDA) and nitric oxide (NO) levels with concurrent depletion of antioxidants (reduced glutathione [GSH], glutathione peroxidase [GPx], glutathione reductase [GR], superoxide dismutase [SOD], catalase [CAT]) and nuclear factor erythroid 2-related factor 2 (Nrf2) downregulation. Inflammatory responses were marked by elevated interleukin-1 beta (IL-1β), tumor necrosis factor-alpha (TNF-α) and nuclear factor kappa B (NF-κB). AFB1 triggered apoptosis via increased caspase-3 and Bcl-2-associated X protein (Bax) with decreased B-cell lymphoma 2 (Bcl-2) expression. Histopathology revealed severe hepatocellular damage including necrosis, vacuolar degeneration and megalocyte formation. Piperine co-treatment significantly attenuated these alterations, restoring liver function parameters, enhancing antioxidant defenses, suppressing inflammatory mediators and normalizing apoptotic markers while preserving hepatic architecture.
Aflatoxin B1, Apoptosis, Hepatotoxicity, Inflammation, Oxidative stress, Piperine