Volume 6, Issue 3 (Summer 2015 -- 2015)                   BCN 2015, 6(3): 171-178 | Back to browse issues page

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Eftekhar-Vaghefi S, Esmaeili Mahani S, Elyasi L, Abbasnejad M. Involvement of Mu Opioid Receptor Signaling in The Protective Effect of Opioid against 6-Hydroxydopamine-Induced SH-SY5Y Human Neuroblastoma Cells Apoptosis. BCN 2015; 6 (3) :171-178
URL: http://bcn.iums.ac.ir/article-1-548-en.html
1- Shahid Bahonar University of Kerman. Kerman, Iran
2- Shahid Bahonar University of Kerman
3- Neuroscience Research Center, Institute of Neuropharmacology, Kerman University of Medical Sciences. Kerman, Iran
Abstract:  
Introduction: The neuroprotective role of opioid morphine against 6-hydroxydopamineinduced cell death has been demonstrated. However, the exact mechanism(s) underlying such neuroprotection, especially the role of subtype receptors, has not yet been fully clarified. 
Methods: Here, we investigated the effects of different opioid agonists on 6-OHDA-induced neurotoxicity in human neuroblastoma SH-SY5Y cell line as an in vitro model of Parkinson’s disease. Cell damage was induced by 150 μM 6-OHDA and the cells viability was examined by MTT assay. Intracellular calcium, reactive oxygen species and mitochondrial membrane potential were assessed by fluorescence spectrophotometry method. Immunoblot technique was used to evaluate cytochrome-c and activated caspase-3 as biochemical markers of apoptosis induction. 
Results: The data showed that 6-OHDA caused significant cell damage, loss of mitochondrial membrane potential and increase in intracellular reactive oxygen species and calcium levels as well as activated caspase-3 and cytochrome-c release. Incubation of SH-SY5Y cells with μ-opioid agonists, morphine and DAMGO, but not with δ-opioid agonist, DADLE, elicited protective effect and reduced biochemical markers of cell damage and death. 
Discussion: The results suggest that μ-opioid receptors signaling participate in the opioid neuroprotective effects against 6-OHDA-induced neurotoxicity.
Type of Study: Original | Subject: Behavioral Neuroscience
Received: 2014/11/11 | Accepted: 2015/05/21 | Published: 2015/07/1

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