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Taurine attenuates amyloid β 1-42-induced mitochondrial dysfunction by activating of SIRT1 in SK-N-SH cells.

Research paper by Qinru Q Sun, Haitao H Hu, Weixi W Wang, Hui H Jin, Gaifeng G Feng, Ning N Jia

Indexed on: 17 Apr '14Published on: 17 Apr '14Published in: Biochemical and Biophysical Research Communications



Abstract

Amyloid β (Aβ) plays a critical role in the pathogenesis of Alzheimer disease (AD). Studies indicate that Aβ causes reactive oxygen species (ROS) generation, mitochondrial dysfunction and neurons loss in vivo and in vitro. Taurine, a naturally occurring β-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 Aβ1-42-treated SK-N-SH cells were investigated. Pretreatment of taurine significantly attenuated Aβ1-42-induced neuronal death. Similarly, taurine suppressed the mPTP opening and reversed mitochondrial function in the presence of Aβ1-42. Additionally, taurine attenuated the intracellular Ca(2+) and ROS generation induced by Aβ1-42. Moreover, the expression of Sirtuin 1 (SIRT1) was obviously recovered by taurine in Aβ1-42-treated SK-N-SH cells. Our results suggest that taurine prevents Aβ1-42-induced mitochondrial dysfunction by activation of SIRT1. This study implies that taurine is a prospective additive for AD patients.