Matrix Science Pharma (MSP)

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

February 25, 2026 Posted by Basem In Uncategorized

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

Journal: Matrix Science Pharma (MSP)
Onyekweli Chinedu Charles, Ben‑Azu Benneth, Nwangwa E. Kingsley, Oyovwi O. Mega

This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited

DOI: 10.4103/mtsp.mtsp_4_25

ABSTRACT

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.

 

Pages 139-150
Year 2025
Issue 4
Volume 9

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