Biochemical and Biophysical Research Communications, Vol.447, No.3, 485-489, 2014
Taurine attenuates amyloid beta 1-42-induced mitochondrial dysfunction by activating of SIRT1 in SK-N-SH cells
Amyloid 3 (AN plays a critical role in the pathogenesis of Alzheimer disease (AD). Studies indicate that All causes reactive oxygen species (ROS) generation, mitochondrial dysfunction and neurons loss in vivo and in vitro. Taurine, a naturally occurring beta-amino acid in the brain, has been demonstrated to have neuroprotective properties. In the present study, the effects of taurine on cell viability and mitochondrial function in A beta 1-42-treated SK-N-SH cells were investigated. Pretreatment of tatirine significantly attenuated A beta-42-induced neuronal death. Similarly, taurine suppressed the mPTP opening and reversed mitochondrial function in the presence of A beta 1-42. Additionally, taurine attenuated the intracellular Ca2+ and ROS generation induced by A beta 1-42. Moreover, the expression of Sirtuin 1 (SIRT1) was obviously recovered by taurine in A beta 1-42-treated SK-N-SH cells. Our results suggest that taurine prevents A beta 1-42-induced mitochondrial dysfunction by activation of SIRT1. This study implies that taurine is a prospective additive for AD patients. (C) 2014 Elsevier Inc. All rights reserved.
Keywords:Amyloid beta;Taurine;Calcium;Reactive oxygen species;Mitochondrial permeability transition pore;Sirtuin 1