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.
نوع مطالعه:
Original |
موضوع مقاله:
Behavioral Neuroscience دریافت: 1393/8/20 | پذیرش: 1394/2/31 | انتشار: 1394/4/10