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논문 기본 정보

자료유형
학술저널
저자정보
Choi, Yong-Jun (Department of Pharmacology, College of Medicine, Kangwon National University) Kwak, Eun-Bee (Department of Pharmacology, College of Medicine, Kangwon National University) Lee, Jae-Won (Department of Pharmacology, College of Medicine, Kangwon National University) Lee, Yong-Suk (Department of Anesthesiology, College of Medicine, Kangwon National University) Cheong, Il-Young (Department of Anesthesiology, College of Medicine, Kangwon National University) Lee, Hee-Jae (Department of Pharmacology, College of Medicine, Kangwon National University) Kim, Sung-Soo (Department of Pharmacology, College of Medicine, Kangwon National University) Kim, Myong-Jo (Division of Bio-resources Technology, Kangwon National University) Kwon, Yong-Soo (College of Pharmacy, Kangwon National University) Chun, Wan-Joo (Department of Pharmacology, College of Medicine, Kangwon National University)
저널정보
한국응용약물학회 Biomolecules & Therapeutics(구 응용약물학회지) Biomolecules & therapeutics 제19권 제2호
발행연도
2011.1
수록면
195 - 200 (6page)

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Neuronal cell death is a common characteristic feature of a variety of neurodegenerative disorders including Alzheimer's disease and Parkinson's disease. However, there have been no effective drugs to successfully prevent neuronal death in those diseases. In the present study, docosyl cafferate (DC), a derivative of caffeic acid, was isolated from Rhus verniciflua and its protective effects on tBHP-induced neuronal cell death were examined in SH-SY5Y human neuroblastoma cells. Pretreatment of DC significantly attenuated tBHP-induced neuronal cell death in a concentration-dependent manner. DC also significantly suppressed tBHP-induced caspase-3 activation. In addition, DC restored tBHP-induced depletion of intracellular Bcl-2, an anti-apoptotic member of the Bcl-2 family. Furthermore, DC significantly suppressed tBHP-induced degradation of IKB, which retains $NF-{\kappa}B$ in the cytoplasm, resulting in the suppression of nuclear translocation of $NF-{\kappa}B$ and its subsequent activation. Taken together, the results clearly demonstrate that DC exerts its neuroprotective activity against tBHP-induced oxidative stress through the suppression of nuclear translocation of $NF-{\kappa}B$.

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