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학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
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연구자들이 자신의 연구와 전문성을 널리 알리고, 새로운 협력의 기회를 만들 수 있는 네트워킹 공간이에요.
논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2007.3
- 수록면
- 33 - 38 (6page)
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초록· 키워드
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Zinc is an endogenous transition metal that can be synaptically released during neuronal activity. However, zinc may contribute to the neuropathology associated with a variety of conditions. Carnosine expressed in glial cells can modulate the effects of zinc on neuronal excitability as a zinc chelator. We hypothesize that carnosine may protect against neurotoxicity of zinc in cortical neuronal cells. The cortical neuronal cells from newborn rats were prepared and exposed to zinc chloride and/or carnosine at various concentrations. Zinc at the doses of 0 to 500 μM decreased neuronal cell viability in a dosedependent manner. Additionally, at the concentrations of 100 and 200 μM, it significantly decreased cell viability in an exposed time-dependent manner (p ＜ 0.05). Treatment with carnosine at the concentrations of 20 and 200 μM significantly increased neuronal cell proliferation by approximately 14% and 20%, respectively, compared to the control (p ＜ 0.05). At the concentrations of 100 and 200 μM zinc, 20 μM carnosine significantly increased the viability of neuronal cells by 18.3% and 12.1%, and 200 μM carnosine also increased it by 33.5% and 28.6%, respectively, compared to the normal control group (p ＜ 0.01). These results suggest that carnosine at a physiologically relevant level may protect against zinc-mediated toxicity in neuronal cells as an endogenous neuroprotective agent.
목차
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
ACKNOWLEDGMENT
REFERENCES
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UCI(KEPA) : I410-ECN-0101-2009-513-016602089