ABSTRACT
Introduction: The neuroprotective role of opioid morphine against 6-hydroxydopamine-induced 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 micro M 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 sigma -opioid agonists, morphine and DAMGO, but not with sigma-opioid agonist, DADLE, elicited protective effect and reduced biochemical markers of cell damage and death
Discussion: The results suggest that sigma-opioid receptors signaling participate in the opioid neuroprotective effects against 6-OHDA-induced neurotoxicity