摘要 : beta-Amyloid peptide (Abeta) was used to induce apoptosis in PC12 cells differentiated by nerve growth factor, and the protective activities of maslinic acid (MA) at 2-16 mu M were examined. Abeta treatment lowered Bcl-2 expressio... 展开 beta-Amyloid peptide (Abeta) was used to induce apoptosis in PC12 cells differentiated by nerve growth factor, and the protective activities of maslinic acid (MA) at 2-16 mu M were examined. Abeta treatment lowered Bcl-2 expression, raised Bax expression, and decreased cell viability. MA pretreatments decreased Bax expression, raised the Bcl-2/Bax ratio, and increased cell viability. MA pretreatments retained glutathione content and decreased subsequent Abeta-induced release of reactive oxygen species, tumor necrosis factor-alpha, interleukin (IL)-1 beta, and IL-6. Abeta treatment up-regulated protein expression of p47(phox) gp91(phox), mitogen-activated protein kinase, advanced glycation end product receptor (RAGE), and nuclear factor-kappa B (NF-kappa B). MA pretreatments at 2-16 mu M suppressed the expression of proteins including gp91(phox), p47(phox), 36 and NF-kappa B p65, at 4-16 mu M down-regulated RAGE and NF-kappa B p50 expression, and at 8 and 16 mu M reduced p-ERK1/2 expression. These novel findings suggest that maslinic acid is a potent compound against Abeta-induced cytotoxicity. 收起