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논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 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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