Selenium and Zinc against Aβ25-35-Induced Cytotoxicity and Tau Phosphorylation in PC12 Cells and Inhibits γ-cleavage of APP.

摘要: Amyloid beta (Aβ) is the main component of amyloid plaques that accumulate in brains Alzheimer patients. The present study was conducted to investigate whether combined treatment with selenium (Se) and zinc (Zn) offers more beneficial effects than provided by either them alone reversing Aβ25–35-induced neurotoxicity PC12 cells. Cells were pretreated 0.1 μmol/L Se Zn for 4 h, after treated 10 mmol/L Aβ25–35 24 h. divided into control five groups, received Aβ25–35,10 mmol/L Aβ25–35 + 0.1 μmol/L Se, Zn, 10 mmol/LAβ25–35 + 0.1 μmol/L Se + 0.1 μmol/L or Zn. result showed cell viability decreased MTT metabolic rate; LDH release MDA, H2O2, NO levels increased GSK-3β phosphorylated tau protein level Aβ25–35-treated group (P < 0.05 P < 0.01), which whole changes attenuated In order evaluate have an effect on processing pathway precursor (APP), we examined activity γ-secretase primary cultured cortical neuron ELISA analysis could inhibit γ-secretase. Then also investigated Aβ1–40 concentration APP-N-terminal fragment expression from APP695 stably transfected Chinese hamster ovary (CHO) CHO cells Zn; four 0.5 M DAPT, decrease production increase expression. These experiments indicate a protective AD pathology possible mechanism inhibiting decreasing further influencing APP processing. Altogether, our findings may provide novel therapeutic target treat sufferers.