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

ABSTRACT

Amyloid ß (Aß) plays a critical role in the pathogenesis of Alzheimer disease (AD). Studies indicate that Aß causes reactive oxygen species (ROS) generation, mitochondrial dysfunction and neurons loss in vivo and in vitro. Taurine, a naturally occurring ß-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 Aß1-42-treated SK-N-SH cells were investigated. Pretreatment of taurine significantly attenuated Aß1-42-induced neuronal death. Similarly, taurine suppressed the mPTP opening and reversed mitochondrial function in the presence of Aß1-42. Additionally, taurine attenuated the intracellular Ca(2+) and ROS generation induced by Aß1-42. Moreover, the expression of Sirtuin 1 (SIRT1) was obviously recovered by taurine in Aß1-42-treated SK-N-SH cells. Our results suggest that taurine prevents Aß1-42-induced mitochondrial dysfunction by activation of SIRT1. This study implies that taurine is a prospective additive for AD patients.