Effects Cycloastragenol on an in vitro Parkinson's Disease Model

Autor: Asli Dogan, Seyma Tasdemir, Erdal Bedir, Aylin Sendemir Urkmez
Rok vydání: 2016
Předmět:
DOI: 10.5281/zenodo.154344
Popis: Parkinson's Disease (PD) is one of the most common movement disorder and the second most common neurodegenerative disease, which is characterized by degeneration of neurons and decline of dopamine secretion [1]. As a dopaminergic disease (in catecholamine dysregulation), PD is a highly idiopathic pathophysiology that occurs because of genetic and epigenetic interactions. The role of oxidative stress, defined as loss of dopaminergic neurons due to free oxygen radicals (ROS), is indicated on the pathophysiologic mechanism of PD [2,3,4]. To prevent the harmful effects of ROS, antioxidant drugs that can scavenge and control the formation of free radicals are under development [4]. Natural secondary metabolites, saponines and saponine-derived compounds have antioxidant properties as well as anti-tumor, immune stimulant, neuroprotective and anti-viral properties [5,6,7]. In this study, PD was modelled in vitro using SH-SY5Y neuroblastoma cell line. Traditional 2D and a realistic 3D cell culture system using 3D Petri Dish technique were employed to construct the in vitro disease model [8]. Cellular viability, cytotoxicity and neuronal morphology were investigated. We have shown that cycloastragenol (CG), one of the saponines, has neuroprotective effects against 6-OHDA induced oxidative stress, and it promotes neuroregeneration. Our results indicate that CG can be further investigated as an alternative drug against PD. We continue our studies to determine the molecular mechanisms of how CG effects dopamine secretion, synaptogenesis. References [1] Iversen, S. D. and Iversen, L. L. (2007), Trends Neurosci.;30(5):188-93. [2] Uttara, B. et al. (2009), Curr Neuropharmacol.; 7(1): 65?74. [3] Dias, V. et al. (2013), J Parkinsons Dis.; 3(4): 461?491. [4] Freeman L. R. and Keller J. N. (2012), Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease; 1822(5), Pages 822?829. [5] Tian, Q. E. et al. (2012), World J Gastroenterol. ;18(47):7079-86. [6] Zhang, X. et al. (2013), Neural Regen Res.; 8(24): 2256?2265. [7] Zhang, W. J. and Frei, B. (2015), Mediators Inflamm. 2015; 2015: 274314. [8] Napolitano, A.P., et al. (2007), Tissue Engineering, 13(8), 2087-2094.
Databáze: OpenAIRE