Borneol alleviates oxidative stress via upregulation of Nrf2 and Bcl-2 in SH-SY5Y cells

Context: The beta-amyloid (A beta) peptide aggregation with accompanying oxidative stress plays the major role in the pathogenesis of Alzheimer's disease (AD). Some natural compounds, including borneol, shed promising light on AD treatment. Objective: The present study was designed to investigate the antioxidative, antiapoptotic effects, and neuroprotection of borneol in human neuroblastoma cells (SH-SY5Y). Materials and methods: Oxidative stress was induced by administering 50 mu M A beta into SH-SY5Y cells. Neuroprotective effect of commercially available borneol was examined by determining cell viability with the MTT assay. Intracellular reactive oxygen species (ROS) generation was measured using a fluorometer with further examination of heme oxygenase-1 (HO-1) and nuclear factor-erythroid 2 p45-related factor 2 (Nrf2) expression. Apoptosis was examined by measuring the ratio of B-cell lymphoma 2 (Bcl-2)/Bcl-2-associated X protein (Bax). Results: Our data indicated that A beta-induced cell cytotoxicity was inhibited by 100 mu M of (-) and (+) borneol treatment. Treatment of borneol significantly decreased ROS generation (P < 0.01). The expression of HO-1 and nuclear translocation of Nrf2 were increased by A beta treatment. This nuclear translocation of Nrf2 was further increased by administration of borneol. Compared with the A beta treated group, the (+) borneol treated group significantly increased Bcl-2 expression with decreased expression of Bax. Discussion and conclusion: Borneol protected SH-SY5Y cells against A beta-induced toxicity, exerted an antioxidative effect and suppressed apoptosis. It increases our knowledge about neuroprotective mechanism of borneol, and it is hopeful to be a candidate compound for developing therapeutic drug for the prevention and treatment of AD and other A beta-related neurodegenerative diseases.