ERYTHROPOIETIN (EPO) AND HIPPOCAMPAL NEURONS: EFFECTS ON SPORTS PERFORMANCE, FITNESS, AND FOOTBALL PLAYERS WITH VASCULAR COGNITIVE IMPAIRMENT

Authors

  • Zhipeng Tang Department of Neurology, Hebei Medical University, Shijiazhuang, Hebei, China
  • Qian Zhang Department of Gastrointestinal Surgery, Beijing Tsinghua Chang Gung Hospital, Beijing, China
  • Yangqing Tie Department of Laboratroy, Hebei General Hospital, Shijiazhuang, Hebei, China
  • Nan Yin Department of Neurology, Hebei General Hospital, Shijiazhuang, Hebei, China
  • Lei Gao Department of Orthopedic, Beijing Shijitan Hospital, Beijing, China
  • Xiaoli Niu Department of Laboratroy, Hebei General Hospital, Shijiazhuang, Hebei, China
  • Sheng Chang Department of Laboratroy, Hebei General Hospital, Shijiazhuang, Hebei, China
  • Xiaozheng Gu Department of Neurology, Hebei Medical University, Shijiazhuang, Hebei, China
  • Peiyuan Lv Department of Neurology, Hebei General Hospital, Shijiazhuang, Hebei, China

Keywords:

Football players, Athletes, Fitness, the PI3K/AKT signaling pathway, vascular dementia, hippocampus, apoptosis and autophagy, oxidative stress, miR-29

Abstract

Objective: This study delves into the impact of erythropoietin (EPO) on hippocampal neurons and its potential implications for sports performance, fitness, and the cognitive well-being of football players facing vascular cognitive impairment.

Methodology: The study employs a comprehensive approach, utilizing a rat model of vascular dementia (VaD) induced by bilateral carotid artery ligation. Exogenous EPO is administered to the VaD rat model. Observations of EPO's influence on hippocampal neurons are made, and in vitro experiments are conducted to validate the specific mechanisms at play, particularly under oxygen/glucose-deprived conditions.

Results: The results reveal several noteworthy findings. VaD rats treated with EPO demonstrate significantly shorter escape latency, increased neuronal populations, and enhanced preservation of Nissl bodies in hippocampal subfields, specifically cortical area 1 (CA1) and CA2. Moreover, these rats exhibit a lower count of TUNEL-positive cells compared to the model group, with higher doses of EPO demonstrating more notable improvements in escape latency. Molecular analysis shows that EPO up-regulates key protein expressions, including phosphorylated EPO receptor (p-EPOR), p-phosphatidylinositol 3-kinase (p-PI3K), p-protein kinase B (Akt), and p-cyclic AMP response element binding protein (p-CREB). Simultaneously, it down-regulates expressions of apoptosis- and autophagy-related proteins, such as B-cell lymphoma-2-associated X protein (Bax), cleaved-Caspase 3, cleaved-Caspase 9, light chain 3β (LC3β), Beclin, autophagy-related gene 5 (ATG5), and ATG7. Notably, in vitro experiments confirm the role of the PI3K/AKT pathway in EPO's mechanisms, with implications for cognitive health.

Conclusion: These findings suggest that EPO may hold promise as a potential intervention to suppress apoptosis and autophagy in hippocampal neurons affected by vascular cognitive impairment. The broader implications extend to sports performance and fitness, particularly for football players who rely on cognitive and physical prowess. Addressing cognitive health alongside physical fitness may yield innovative strategies for enhancing athletic performance and the well-being of athletes facing cognitive challenges. Further research in this direction could pave the way for novel approaches to optimize both physical and cognitive aspects of sports performance in football and beyond.

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Published

2023-10-19

Issue

Vol. 23 No. 91 (2023): Vol. 23, No. 91, Julio / July 2023

Section

Articles