Salidroside Protects Caenorhabditis elegans Neurons from Polyglutamine-Mediated Toxicity by Reducing Oxidative Stress

Molecules

Lingyun Xiao³  Haifeng Li³  Ju Zhang³  Fan Yang³  Aizhen Huang¹  Jingjing Deng³  Ming Liang²  Fangli Ma²  Minghua Hu² 

[1] Guangdong Province Key Laboratory for Biotechnology Drug Candidates, School of Biosciences and Biopharmaceutics, Guangdong Pharmaceutical University, Guangzhou 510006, China; E-Mail:;Research & Development Centre, Infinitus (China) Company Ltd, Guangzhou 510665, China; E-Mails:;School of Pharmaceutical Sciences, Wuhan University, Wuhan 430071, China; E-Mails:

关键词: salidroside;    polyglutamine;    neurotoxicity;    oxidative stress;    C. elegans;    chemoavoidance;   

DOI  :  10.3390/molecules19067757

来源: mdpi

【 摘 要 】

Polyglutamine (polyQ) aggregation plays a pivotal role in the pathological process of Huntington’s disease and other polyQ disorders. Therefore, strategies aiming at restoring dysfunction and reducing stresses mediated by polyQ toxicity are of therapeutic interest for proteotoxicity diseases. Salidroside, a glycoside from Rhodiola rosea, has been shown to have a variety of bioactivities, including antioxidant activity. Using transgenic Caenorhabditis elegans models, we show here that salidroside is able to reduce neuronal death and behavioral dysfunction mediated by polyQ expressed in ASH neurons, but the neuroprotective effect is not associated with prevention of polyQ aggregation per se. Further experiments reveal that the neuroprotective effect of salidroside in C. elegans models involves its antioxidant capabilities, including decrease of ROS levels and paraquat-induced mortality, increase of antioxidant enzyme activities and reduction of lipid peroxidation. These results demonstrate that salidroside exerts its neuroprotective function against polyQ toxicity via oxidative stress pathways.

【 授权许可】

CC BY   
© 2014 by the authors; licensee MDPI, Basel, Switzerland.