ABSTRACT
EPIGALLOCATECHIN-3-GALLATE ATTENUATED AUTOPHAGY EXACERBATED HIGH FAT DIET-INDUCED MEMORY AND TESTICULAR TOXICITY IN RATS: THE FUNCTION OF INFLAMMATORY AND MTOR SIGNALING PATHWAYS
Journal: Matrix Science Pharma (MSP)
Author: 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: 10.26480/msp.01.2026.22.31
The study evaluated the potential effects of epigallocatechin-gallate (EGCG) against high-fat diet (HFD)-induced memory decline and testicular abnormalities. Thirty-six (36) research rats divided into six groups with six rats each were utilized. DMSO (0.1 %) and EGCG (80 mg/kg) were administered to group 1 and 2, respectively. Groups 3 and 4 were treated with HFD and HFD plus rapamycin for 56 days. DMSO or EGCG (80 mg/kg) was given to groups 5 and 6 for 29-56 days, respectively. However, animals in groups 5–6 were treated with HFD and HFD plus rapamycin individually for 56 days. The study investigated the cognitive capacity of the rats using novel-object recognition tests. The adrenal gland and prefrontal cortex of the rat testes and brain were assessed for inflammatory, autophagic state, neurochemical, and histological alterations. All rats had their serum leptin, adiponectin, and corticosterone evaluated. The findings demonstrated that HFD consumption resulted in cognitive deterioration, an imbalance of inflammatory cytokines, an increase in the lee index, and neuronal death. But in the HFD-exposed rats, EGCG therapy reduced corticosterone, leptin, and lee index, improved cognitive impairment, regulated inflammatory, autophagic, and apoptotic status, elevated adiponectin, increased brain-testes weight, and protected neuronal atrophy. Accordingly, EGCG reduced the negative effects of an HFD-induced non-spatial memory and testicular dysfunctions, possibly by reducing hypercortisolism, controlling chemo-brain activity, regulating inflammatory, apoptotic, autophagic, and metabolic hormonal status, and preventing neuronal degeneration.
| Pages | 22-31 |
| Year | 2026 |
| Issue | 1 |
| Volume | 10 |


