Inhibitory Effect of Piperlonguminine/Dihydropiperlonguminine on the Production of Amyloid β and APP in SK-N-SH Cells

Hong-Shun Qi ； Pei Liu ； Su-Qin Gao ； Zeng-Yan Diao ； Ling-Ling Yang ； Jun Xu ； Xun Qu ； En-Ji Han

《The Chinese Journal of Physiology》 52卷3期 (2009/06) Pp. 160-168

https://doi.org/10.4077/CJP.2009.AMH062

並列摘要

The study was undertaken to explore whether piperlonguminine/dihydropiperlonguminine could inhibit the production of amyloidβ (Aβ) in human neuroblastoma cells (SK-N-SH) and to examine the underlying mechanism of this effect. Piperlonguminine/dihydropiperlonguminine components (1:0.8) were extracted from Futokadsura stem, and then used to treat SK-N-SH cells at three different concentrations: 3.13 μg/ml, 6.25 μg/ml and 12.50 μg/ml. Subsequently, the production of Aβ42 and Aβ40 were measured by Western blot analysis and enzyme linked immunosorbent assay (ELISA). On the other hand, the expressions of amyloid precursor protein (APP), Notch1 (Notch intracellular domain) and β-site amyloid precursor protein cleavage enzyme (BACE-1) were also examined by Western blot assay. The activities of β-secretase and γ-secretase were detected at the same time. Furthermore, Aβ42 level was detected by immunocytochemistry staining. We demonstrated that the treatment of piperlonguminine/dihydropiperlonguminine could significantly decrease the levels of APP, Aβ42 and Aβ40 peptide in SK-N-SH cells, despite the fact that the activities of β-secretase and γ-secretase were not affected significantly. These data suggest that piperlonguminine/dihydropiperlonguminine components could significantly inhibit the level of APP, Aβ42 and Aβ40 peptide without affecting the activity of β-secretase and γ-secretase in SK-N-SH cells.

並列關鍵字

Alzheimer disease ； amyloid precursor protein ； amyloid β ； β-secretase ； γ-secretase ； piperlonguminine ； dihydropiperlonguminine ； futokadsura stem

參考文獻

Findeis, M.A.(2007).The role of amyloid β peptide 42 in Alzheimer's disease.Pharmacol. Ther..116,266-286.

Findeis, M.A.(2007).The role of amyloid β peptide 42 in Alzheimer's disease.Pharmacol. Ther..116,266-286.

Forero, D.A.,Casadesus, G.,Perry, G.,Arboleda, H.(2006).Synaptic dysfunction and oxidative stress in Alzheimer's disease: emerging mechanisms.J. Cell Mol. Med..10,796-805.

Forero, D.A.,Casadesus, G.,Perry, G.,Arboleda, H.(2006).Synaptic dysfunction and oxidative stress in Alzheimer's disease: emerging mechanisms.J. Cell Mol. Med..10,796-805.

Goedet, M.,Spillantini, M.G.(2006).A century of Alzheimer's disease.Science.314,777-781.