Cyanidin-3-O-glucoside attenuates amyloid-beta (1–40)-induced oxidative stress and apoptosis in SH-SY5Y cells through a Nrf2 mechanism

Abstract

Scope: We investigated the cytoprotective effects of cyanidin-3-O-glucoside (C3G) against oxidative stress and apoptosis induced by beta-amyloid1-40 (Aβ1-40) in SH-SY5Y cells. Methods and results: We measured intracellular reactive oxygen species (ROS) with fluorescent marker DCFH2-DA, superoxide dismutase (SOD), hydrogen peroxide (H2O2), glutathione peroxidase (GSH-Px) with the kits, and calcium, cellular apoptosis with Fluo-3/AM, annexin-V-FITC staining, respectively. C3G pretreatment significantly inhibited the Aβ1-40-induced increase in intracellular calcium, ROS, H2O2, increased the expression of SOD, GSH-Px and the antioxidant enzyme involved in the C3G’s antioxidant potential, including heme oxygenase-1 (HO-1), quinone oxidoreductase 1(NQO-1) regulated by nuclear factor erythroid 2-related factor-2 (Nrf2). Western blotting, RT-PCR revealed that C3G significantly increased Nrf2, HO-1, NQO-1 expression. Besides, apoptosis was significantly inhibited by C3G via down-regulation of pro-apoptosis factor Bax and up-regulation of anti-apoptosis factor Bcl-2. Conclusion: C3G protects SH-SY5Y cells from Aβ1-40-induced oxidative stress and subsequent apoptosis by regulating cellular antioxidant defenses and apoptosis-related genes.

Keywords

• Cyanidin-3-O-glucoside
• SH-SY5Y cell
• Aβ1-40
• Oxidative stress
• Apoptosis
• NrF2/ARE activation