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자료유형
학술저널
저자정보
Lee, Ah Young (Department of Food Science and Nutrition and Kimchi Research Institute, Pusan National University) Lee, Myoung-Hee (Department of Southern Area Crop Science, National Institute of Crop Science, Rural Development Administration) Lee, Sanghyun (Department of Integrative Plant Science, Chung-Ang University) Cho, Eun Ju (Department of Food Science and Nutrition and Kimchi Research Institute, Pusan National University)
저널정보
한국응용생명화학회 Applied Biological Chemistry Applied Biological Chemistry 제61권 제1호
발행연도
2018.1
수록면
61 - 71 (11page)

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Alpha-linolenic acid (ALA), which is an omega-3 fatty acid from plant oils, has been reported to have beneficial effects on human brain health. However, the protective effect of ALA and its mechanism of action against amyloid beta ($A{\beta}$)-mediated neurotoxicity, neuronal apoptosis and amyloid precursor protein (APP) processing are unclear. To investigate the neuroprotective effect of ALA, we treated $A{\beta}_{25-35}$-induced SH-SY5Y cells with ALA (1, 2.5, 5 and $25{\mu}g/mL$). In our results, $A{\beta}_{25-35}$-induced neuronal cell loss was observed, whereas ALA significantly increased the cell viability and decreased lactate dehydrogenase release. In addition, over-production of reactive oxygen species caused by $A{\beta}_{25-35}$ was attenuated by treatment with ALA, and these inhibitory activities were mediated by regulation of the mitogen-activated protein kinase signaling pathway. Furthermore, our data shows that $A{\beta}_{25-35}$ cause an increase in protein expression of APP-C-terminal fragment ${\beta}$, ${\beta}-site$ APP-cleaving enzyme and presenilin-1 in SH-SY5Y cells, while ALA significantly down-regulated the expression of those amyloidogenic APP processing-related proteins. In addition, we confirmed that ALA enhanced ${\alpha}$-secretase activity by up-regulating the protein levels of A distintegrin and metalloprotease 10 and tumor necrosis factor-${\alpha}$-converting enzyme, indicating that ALA could promote non-amyloidogenic signaling pathways. ALA also significantly attenuated $A{\beta}_{25-35}$-induced neuronal apoptosis by up-regulation of the Bcl-2/Bax ratio. These findings suggest that ALA may be a beneficial agent for promoting prevention of Alzheimer's disease.

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