Anti-aging trait of whey protein against brain damage of senile rats

Abstract

AbstractAging mammalian results in impaired bio-functions and neurological disorders. The current study investigated whether whey protein (WP) syrup supplementation may improve age-related changes in diseased brain indicators like tau protein, β-amyloid and α-amylase. The study was carried out in conjunction with immunohistochemistry, histology, and flow cytometry of apoptosis. At the ages of 8 and 30 months, Wistar albino rats (Rattus novergicus) were divided into four groups (n = 8; G1; 8 months old rats; G2, 8 months old rats supplemented WP; G3, 30 months old rats; G4, 30 months old rats supplemented WP), with or without whey syrup administration. For 2 months, oral whey supplementation in 2 mL/kg doses is given twice a day every 12 h. Rats were sacrificed, and their brains were subjected to biochemical, histological, immunohistochemistry, and flow cytometric investigations. Aged rats had lower levels of superoxide dismutase (SOD), adenosine triphosphate (ATP), serotonin (5-HT), and dopamine (DA). These observations were parallel with increased inflammatory markers [tumor necrosis factor α- and 5-lipoxygenase (5-LO)], lipid peroxidation products (MDA), as well as apoptotic marker caspase-3, annexin-v, tau protein, β-amyloid, and α-amylase. Whey administration to aged rats reduced inflammatory and oxidative stress markers as well as improved neurotransmitters, tau protein, β-amyloid, and α-amylase. The advantages of supplementation were validated by improved histology and immunohistochemistry in aged rats’ cerebrum, cerebellum, and hippocampus. In addition, apoptosis was reduced, according to flow cytometry analysis of annexin-v. In conclusion, WP contains amino acids and bioactive compounds that could decrease brain oxidative stress and restore normal metabolic function. Furthermore, increased antioxidant defense and DA and 5-HT neurotransmitters, while decreasing brain tau protein and β-amyloid, were associated with better histology in aged rats’ cerebrum, cerebellum, and hippocampus.