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자료유형
학술저널
저자정보
Ji Hyun Kim (Gyeongsang National University) Sanghyun Lee (Chung-Ang University) Eun Ju Cho (Pusan National University)
저널정보
충남대학교 농업과학연구소 Korean Journal of Agricultural Science Korean Journal of Agricultural Science Vol.49 No.2
발행연도
2022.6
수록면
227 - 237 (11page)

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Amyloid beta (Aβ) is produced from an amyloid precursor protein by the activation of the amyloidogenic pathway, and it is widely known to cause Alzheimer’s disease (AD). In this study, we investigated the neuroprotective effects of three flavonoids, quercitrin, isoquercitrin, and afzelin, from Acer okamotoanum against Aβ-induced neurotoxicity in SHSY5Y neuronal cells. Aβ<SUB>25-35</SUB> treatments resulted in decreased cell viability and increased levels of nuclei condensation and fragmentation. However, an isoquercitrin treatment dosedependently increased cell viability and decreased nuclei condensation and fragmentation levels. SH-SY5Y cells treated with Aβ<SUB>25-35</SUB> showed increased reactive oxygen species (ROS) production compared to that from cells not treated with Aβ<SUB>25-35</SUB>. However, treatment with the three flavonoids significantly inhibited ROS production compared to an Aβ<SUB>25-35</SUB>-treated control group, indicating that the three flavonoids blocked neuronal oxidative stress. For a closer examination of the neuroprotective mechanisms, we measured the expressions of the non-amyloidogenic pathway-related proteins of a disintegrin and metalloprotease 10 (ADAM10) and the tumor necrosis factor-α converting enzyme (TACE). An isoquercitrin treatment enhanced the expressions of ADAM10 compared to the control group. In addition, the three flavonoids activated the non-amyloidogenic pathway via the upregulation of TACE. In conclusion, we demonstrated neuroprotective effects of three flavonoids from A. okamotoanum, in particular isoquercitrin, on neurotoxicity by the regulation of the nonamyloidogenic pathway in Aβ<SUB>25-35</SUB><SUB></SUB>-treated SH-SY5Y cells. Therefore, we suggest that flavonoids from A. okamotoanum may have some potential as therapeutics of AD.

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Abstract
Introduction
Materials and Methods
Results and Discussion
Conclusion
References

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