Rhodiola rosea Extract Protects Human Cortical Neurons against Glutamate and Hydrogen Peroxide-induced Cell Death Through Reduction in the Accumulation of Intracellular Calcium
Article first published online: 15 NOV 2011
Copyright © 2011 John Wiley & Sons, Ltd.
Volume 26, Issue 6, pages 878–883, June 2012
How to Cite
Palumbo, D. R., Occhiuto, F., Spadaro, F. and Circosta, C. (2012), Rhodiola rosea Extract Protects Human Cortical Neurons against Glutamate and Hydrogen Peroxide-induced Cell Death Through Reduction in the Accumulation of Intracellular Calcium. Phytother. Res., 26: 878–883. doi: 10.1002/ptr.3662
- Issue published online: 4 JUN 2012
- Article first published online: 15 NOV 2011
- Manuscript Accepted: 29 AUG 2011
- Manuscript Revised: 29 JUL 2011
- Manuscript Received: 23 JUN 2011
- Rhodiola rosea L. (Crassulaceae);
- human cortical neuron;
- oxidative stress;
- intracellular calcium;
The aim of this study was to investigate the neuroprotective effects of a titolated extract from Rhodiola rosea L. (RrE) and of salidroside (Sa), one of the major biologically active compounds extracted from this medicinal plant, against oxidative stressor hydrogen peroxide (H2O2) and glutamate (GLU)-induced cell apoptosis in a human cortical cell line (HCN 1-A) maintained in culture. The results obtained indicate that exposure of differentiated HCN 1-A neurons to GLU or H2O2 resulted in concentration-dependent cell death. A 24 h pre-treatment with RrE significantly increased cell survival and significantly prevented the plasma membrane damage and the morphological disruption caused by GLU or H2O2, indicating that neurons treated with RrE were protected from the neurotoxicity induced by the oxidative stressor used. In addition, RrE significantly reduced H2O2 or GLU-induced elevation of intracellular free Ca2+ concentration. The results obtained have also shown that Sa caused similar effects in all experimental models used; however, the potency of the action was lower than that of the extract containing corresponding quantities of Sa. These findings indicate that RrE has a neuroprotective effect in cortical neurons and suggest that the antioxidant activity of the RrE, due to the structural features of the synergic active principles they contain, may be responsible for its ability to stabilize cellular Ca2+ homeostasis. Copyright © 2011 John Wiley & Sons, Ltd.