The study was undertaken to explore whether
piperlonguminine/dihydropiperlonguminine could inhibit the production of amyloidbeta (Abeta) 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 microg/ml, 6.25 microg/ml and 12.50 microg/ml. Subsequently, the production of Abeta42 and Abeta40 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 beta-site
amyloid precursor
protein cleavage
enzyme (BACE-1) were also examined by Western blot assay. The activities of
beta-secretase and
gamma-secretase were detected at the same time. Furthermore, Abeta42 level was detected by immunocytochemistry staining. We demonstrated that the treatment of
piperlonguminine/dihydropiperlonguminine could significantly decrease the levels of APP, Abeta42 and Abeta40
peptide in SK-N-SH cells, despite the fact that the activities of
beta-secretase and
gamma-secretase were not affected significantly. These data suggest that
piperlonguminine/dihydropiperlonguminine components could significantly inhibit the level of APP, Abeta42 and Abeta40
peptide without affecting the activity of
beta-secretase and
gamma-secretase in SK-N-SH cells.