Epigallocatechin-3-gallate Attenuated Autophagy Exacerbated High-fat Diet-induced Memory and Testicular Toxicity in Rats: The Function of Inflammatory and Mechanistic Target of Rapamycin Signaling Pathways

Background: High-fat diet (HFD) can induce neuroinflammation, oxidative stress, and reproductive toxicity, which contribute to memory and testicular dysfunctions. Aims and Objectives: To investigate the protective role of epigallocatechin-3-gallate (EGCG) against HFD-induced cognitive and testicular toxicity via inflammatory and mTOR signaling pathways. Materials and Methods: Male Wistar rats were divided into groups receiving normal diet, HFD, or HFD with EGCG treatment. Behavioral, biochemical, and histopathological analyses were performed, and inflammatory and mTOR pathway markers were evaluated. Results: EGCG significantly improved memory and learning performance, reduced oxidative and inflammatory markers, restored testicular histoarchitecture, and modulated mTOR signaling. Conclusion: EGCG attenuates HFD-induced cognitive and testicular impairments through the regulation of inflammation and mTOR signaling, suggesting its therapeutic potential in diet-induced metabolic disorders.