As the irreversible products of the non-enzymatic reduction of sugars and the amino groups of proteins or peptides, advanced glycation end products (AGEs) are metabolized and excreted via the kidneys. However, if AGEs are not metabolized, they are deposited in the kidneys and bind to AGE receptors (RAGE), which can induce various pathological changes, including oxidative stress, apoptosis, and inflammation. This study used the D-galactose (DG)-induced rat model to explore the potential role and mechanism of L-theanine in inhibiting AGEs/RAGE-related signaling pathways in renal tissues. L-theanine increased the activities of glutathione peroxidase (GSH-Px) and total antioxidant capacity (T-AOC) while downregulating the contents of malondialdehyde (MDA) and AGEs in renal tissues induced by DG (P < 0.05). By inhibiting the upregulation of RAGE protein expression attributed to AGEs accumulation (P < 0.05), L-theanine downregulated phosphorylated nuclear factor (p-NF-κB (p65)), Bax, and cleaved-caspase-3 expression and increased Bcl-2 protein expression (P < 0.05), thereby alleviating the oxidative stress damage and reducing the inflammation and cell injury induced by DG. In addition, the Congo red staining section of renal tissue also showed that the natural product L-theanine can protect against AGEs-induced renal damage in DG-induced rat model.
Keywords: AGEs; AGEs/RAGE signaling; L-theanine; Renal injury.
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