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논문 기본 정보

자료유형
학술저널
저자정보
Ju-Bin Kang (Department of Veterinary Medicine College of Veterinary Medicine Research Institute of Life Science Gyeongsang National University) Hyeun-Gyoung (Department of Veterinary Medicine College of Veterinary Medicine Research Institute of Life Science Gyeongsang National University) Dong-Ju Park (Department of Veterinary Medicine College of Veterinary Medicine Research Institute of Life Science Gyeongsang National University) Jae-You Kim (Department of Veterinary Medicine College of Veterinary Medicine Research Institute of Life Science Gyeongsang National University) Hyun-Kyoung Son (Department of Veterinary Medicine College of Veterinary Medicine Research Institute of Life Science Gyeongsang National University) Phil-Ok Koh (Department of Veterinary Medicine College of Veterinary Medicine Research Institute of Life Science Gyeongsang National University)
저널정보
한국예방수의학회 예방수의학회지 예방수의학회지 제47권 제2호
발행연도
2023.6
수록면
49 - 56 (8page)

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Ischemic stroke causes brain damage and neuronal cell death by depriving oxygen and nutrients and releasing excessive levels of glutamate and intracellular calcium. Epigallocatechin gallate (EGCG) is a polyphenolic compound present in green tea. It has antioxidant, anti-inflammatory, and neuroprotective effects. Hippocalcin is a calcium binding protein that regulates calcium concentration, neuronal differentiation, neuronal excitability, and neuronal cell death. In this study, we investigated whether EGCG regulates the expression of hippocalcin in neurons and astrocytes after focal cerebral ischemia. Cerebral ischemia was induced by meddle cerebral artery occlusion (MCAO). EGCG (50 mg/kg) or PBS was injected into the abdominal cavity just before MCAO surgery. Neurobehavioral tests were performed to evaluate the effect of EGCG on neurological behavioral deficits 24 h after MCAO surgery. Immunofluorescence staining was performed to evaluate the positive response to hippocalcin in the cerebral cortex after MCAO surgery. We also detected the positive reactions of neuronal nuclear protein (NeuN) and glial fibrillary acidic protein (GFAP) as markers of neuron and astrocyte, respectively. MCAO caused severe neurological impairment and EGCG treatment attenuated these impairments. MCAO damage reduced the number of NeuN-positive cells and increased the number of GFAP-positive cells. This result indicates a decrease in neurons and an increase in astrocytes. However, EGCG alleviated these changes caused by MCAO damage. MCAO reduced the number of hippocalcin-positive cells in neurons and astrocytes, and EGCG treatment attenuated these reductions. Hippocalcin exerts neuroprotective effect through regulating intracellular calcium concentration. In conclusion, EGCG regulates the expression of hippocalcin in neurons and astrocytes and has neuroprotective effects in focal cerebral ischemia.

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