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자료유형
학술저널
저자정보
Youn, Myung-Ja (Vestibulocochlear Research Center & Department of Microbiology, School of Medicine) Park, Seong-Yeol (Vestibulocochlear Research Center & Department of Microbiology, School of Medicine) Park, Cha-Nny (Vestibulocochlear Research Center & Department of Microbiology, School of Medicine) Kim, Jin-Kyung (Vestibulocochlear Research Center & Department of Microbiology, School of Medicine) Kim, Yun-Ha (Vestibulocochlear Research Center & Department of Microbiology, School of Medicine) Kim, Eun-Sook (Vestibulocochlear Research Center & Department of Microbiology, School of Medicine) Moon, Byung-Soon (School of Oriental Medicine, Wonkwang University) So, Hong-Seob (Vestibulocochlear Research Center & Department of Microbiology, School of Medicine) Park, Raek-Il (Vestibulocochlear Research Center & Department of Microbiology, School of Medicine)
저널정보
대한동의생리학회 동의생리병리학회지 동의생리병리학회지 제22권 제2호
발행연도
2008.1
수록면
438 - 445 (8page)

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Dodam formula (Dodam) has been used for neurodegenerative disease in Oriental medicine. Dodam is capable of protecting diverse kinds of cells from damage caused by a variety of toxic stimuli. In the present study, we investigated the underlying protective mechanism of Dodam on rotenone-induced cytotoxicity in rat neuroblastoma Neuro-2A cells. Treatment with Neuro-2A cells with rotenone caused the loss of cell viability, and condensation and fragmentation of nuclei, which was associated with the elevation of ROS level, and lipid peroxidation, the increase in Bax/Bcl-2 ratio. Rotenone induced mitochondrial dysfunction characterized by mitochondrial membrane potential loss and cytochrome-c release. These phenotypes induced by rotenone were reversed by pretreatment with Dodam. Our results suggested that major features of rotenone-induced neurotoxicity are partially mediated by mitochondrial dysfunction and oxidative stress, and that Dodam markedly protects Neuro-2A cells from oxidative injury. These data indicated that Dodam might provide a useful therapeutic strategy in treatment of the neurodegenerative diseases caused by oxidative injuries.

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