L-Theanine attenuates liver aging by inhibiting advanced glycation end products in D-galactose-induced rats and reversing an imbalance of oxidative stress and inflammation

Redox and inflammation imbalances are associated with increased levels of advanced glycation end products (AGEs), leading to the degeneration of body function. L-Theanine, derived from tea, reportedly inhibits AGE formation in vitro. We investigated the effects on AGE content, oxidative stress, and inflammatory factors in D-galactose-induced aging rats for prevention and treatment of age-related liver dysfunction. L-Theanine increased activities of antioxidant enzymes such as superoxide dismutase, catalase, and glutathione peroxidase, thus enhancing total antioxidant capacity, and decreasing malondialdehyde and nitric oxide synthase levels in serum and liver. Levels of the pro-inflammatory factors, interleukin (IL)-1 beta, tumour necrosis factor-alpha, and IL-6 were decreased in serum and liver, whereas those of anti-inflammatory factors, IL-4 and IL-10, were increased in the serum. Further, L-theanine inhibited AGE production and decreased the levels of the liver function markers, alanine aminotransaminase and aspartate aminotransferase. It also significantly increased the mRNA expression levels of FoxO1 and downregulated NF-kappa B(p65) but suppressed the phosphorylation of both FOXO1 and NF-kappa B (p65). Moreover, L-theanine effectively attenuated n-galactose-induced oedema and vacuole formation, thus protecting the liver. Overall, L-theanine reversed the D-galactose-induced imbalance in oxidative stress and inflammatory responses, reduced AGEs content in aging rats, maintained homeostasis in the body, and ameliorated liver aging.