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Background <p>High-fat diet (HFD) contributes to cognitive and reproductive impairments, yet therapeutic options are limited. This study examines epigallocatechin-gallate (EGCG) for its effects on HFD-induced memory deficits and testicular injury, along with its protective mechanisms.</p> Methods <p>Thirty-six rats were divided into six groups. Groups 1 and 2 received DMSO (0.1%) and EGCG (80&#xa0;mg/kg). Groups 3 and 4 were treated with HFD and HFD + rapamycin for 56&#xa0;days. Groups 5 and 6 received DMSO or EGCG for 29–56&#xa0;days and were also treated with HFD and HFD + rapamycin for 56&#xa0;days. Cognitive capacity was assessed using novel-object recognition tests. The adrenal gland, prefrontal cortex, and striatum were examined for inflammatory, apoptotic, autophagic, neurochemical, and histological changes. Serum leptin, adiponectin, and corticosterone levels were evaluated.</p> Results <p>Results showed that HFD consumption led to cognitive decline, increased Lee index, and neuronal death&#xa0;accompanied by an inflammatory cytokine imbalance. EGCG therapy in HFD rats reduced corticosterone, leptin, and Lee index, improved cognitive function, regulated inflammatory and apoptotic states, increased adiponectin, elevated brain-testicular weight, and protected against neuronal atrophy.</p> Conclusion <p>EGCG mitigated HFD-induced non-spatial memory impairment and testicular dysfunction by decreasing hypercortisolism, regulating chemo-brain activity, and controlling inflammation and hormonal states, thus preventing neuronal degeneration.</p>

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Autophagy-dependent pathways mediate memory and testicular impairments induced by a high-fat diet in rats, which can be reversed by epigallocatechin-3-gallate

  • 期刊论文

  • 发表日期：

    2025年5月5日

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  • Chinedu Charles Onyekweli,
  • Benneth Ben-Azu,
  • Kingsley E. Nwangwa,
  • Mega O. Oyovwi,
  • Julian E. Nwangwa,
  • Ejime Agbonifo-Chijiokwu,
  • Simon I. Ovuakporaye,
  • Oghenetega B. Onome,
  • Shalom U. Nwabuoku,
  • Rume A. Rotu,
  • Joseph G. Uchechukwu

摘要

Background

High-fat diet (HFD) contributes to cognitive and reproductive impairments, yet therapeutic options are limited. This study examines epigallocatechin-gallate (EGCG) for its effects on HFD-induced memory deficits and testicular injury, along with its protective mechanisms.

Methods

Thirty-six rats were divided into six groups. Groups 1 and 2 received DMSO (0.1%) and EGCG (80 mg/kg). Groups 3 and 4 were treated with HFD and HFD + rapamycin for 56 days. Groups 5 and 6 received DMSO or EGCG for 29–56 days and were also treated with HFD and HFD + rapamycin for 56 days. Cognitive capacity was assessed using novel-object recognition tests. The adrenal gland, prefrontal cortex, and striatum were examined for inflammatory, apoptotic, autophagic, neurochemical, and histological changes. Serum leptin, adiponectin, and corticosterone levels were evaluated.

Results

Results showed that HFD consumption led to cognitive decline, increased Lee index, and neuronal death accompanied by an inflammatory cytokine imbalance. EGCG therapy in HFD rats reduced corticosterone, leptin, and Lee index, improved cognitive function, regulated inflammatory and apoptotic states, increased adiponectin, elevated brain-testicular weight, and protected against neuronal atrophy.

Conclusion

EGCG mitigated HFD-induced non-spatial memory impairment and testicular dysfunction by decreasing hypercortisolism, regulating chemo-brain activity, and controlling inflammation and hormonal states, thus preventing neuronal degeneration.