Changes in hippocalcin expression in cortical neurons and glial cells by epigallocatechin gallate administration in an animal model of stroke

서지정보

· 발행기관 : 한국예방수의학회(구 한국수의공중보건학회)
· 수록지 정보 : 예방수의학회지 / 47권 / 2호
· 저자명 : Ju-Bin Kang, Dong-Ju Park, Jae-You Kim, Hyun-Kyoung Son, Phil-Ok Koh

목차

서 론
재료 및 방법
실험동물
중간대뇌동맥폐쇄 (middle cereberal artery occlusion,MCAO)
신경 결손 테스트 (Neurological deficit scoring test)
코너 테스트 (Corner test)
악력 테스트 (Grip strength test)
접착제 제거 체성 감각 테스트 (Adhesive removalsomatosensory test)
면역형광염색 (immunofluorescence stain)
통계 분석
결 과
허혈성 뇌 손상 시 EGCG 투여에 의한 신경행동학적기능장애 완화 관찰
허혈성 뇌 손상 시 EGCG 투여에 의한 hippocalcin 양성반응 세포 수의 변화 관찰
허혈성 뇌 손상 시 EGCG 투여에 의한 NeuN 및 GFAP양성반응 세포 수의 변화 관찰
고 찰
감사의 글

영어초록

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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