Protective effect of orexin-A on 6-hydroxydopamine-induced neurotoxicity in SH-SY5Y human dopaminergic neuroblastoma cells

Esmaeili‐Mahani, Saeed; Vazifekhah, Somayeh; Pasban-Aliabadi, Hamzeh; Abbasnejad, Mehdi; Sheibani, Vahid

doi:10.1016/j.neuint.2013.09.022

Cited by 32 publications

(25 citation statements)

References 39 publications

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“…Thus, 50 µM rotenone was used to induce cellular damage for further analysis. Consistent with previous studies, we observed significant decreases in cell viability following paraquat or 6-OHDA treatments at different time points [33][34][35]. It is suggested that performing dose-response studies while studying, particularly, rotenone-induced neurotoxicity is very important before investigating molecular responses of neurotoxins.…”

Section: Discussionsupporting

confidence: 90%

“…Siddiqui et al (2013) showed that rotenone exposure significantly increased mRNA and protein levels of Bax and p53 as well as decreased mitochondrial membrane potential supporting its mitochondrialtargeted effect [38]. Similarly, it was reported that Bax levels were significantly increased when cells treated with 150 µM 6-OHDA [34]. In our study, the alterations in levels of apoptosis-related proteins were evaluated following neurotoxin treatments.…”

Section: Discussionsupporting

confidence: 61%

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The comparison of apoptosis-related protein expressions in neurotoxin-based in vitro Parkinson s Disease models

Kaftan¹,

Armağan²,

Dağcı³

2020

jrp

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Programmed cell death (apoptosis) is mainly responsible for neuronal damage in neurodegenerative diseases. Thus, inhibition of apoptosis could represent an effective strategy in the prevention of these diseases. In this study, we aimed to compare the apoptotic responses of neurotoxins that are widely used to induce neuronal damage in cell culture studies and help to decide the most suitable experimental model for drug studies that target apoptosis. Cell viability analyses were performed by MTT assay following 1-methyl-4-phenylpyridinium (MPP +), 6-hydroxydopamine (6-OHDA), rotenone and paraquat treatments at three different time points (12, 24, 48h). Pro-apoptotic (Bax, Bad, Bak), anti-apoptotic (Bcl-2, Bcl-xl) protein levels and total caspase-3 protein levels were determined by Western Blotting technique following treatments. As expected, all neurotoxins managed to trigger cell death and apoptotic pathway. On the other hand, each neurotoxin was found to enhance and/or reduce the levels of different proteins that are associated with apoptosis. Due to different responses of apoptosis related proteins to neurotoxins, it can be concluded that the determination of target proteins with a number of protein-binding assays prior to cell culture studies and then deciding an in vitro model are essential while screening newly synthesized drugs that target apoptosis.

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Section: Discussionsupporting

confidence: 90%

Section: Discussionsupporting

confidence: 61%

The comparison of apoptosis-related protein expressions in neurotoxin-based in vitro Parkinson s Disease models

Kaftan¹,

Armağan²,

Dağcı³

2020

jrp

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“…Recent studies have reported that orexin-A exerts a neuroprotective effect in cerebral ischemia and in a cellular model of Parkinson's disease [ 24 25 ]. Orexin-A was also shown to contribute to the protection of gastric mucosa against acute gastric damage [ 26 ].…”

Section: Discussionmentioning

confidence: 99%

Involvement of Heme Oxygenase-1 in Orexin-A-induced Angiogenesis in Vascular Endothelial Cells

Park

Kim

Choi

et al. 2015

Korean J Physiol Pharmacol

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The cytoprotective enzyme heme oxygenase-1 (HO-1) influences endothelial cell survival, proliferation, inflammatory response, and angiogenesis in response to various angiogenic stimuli. In this study, we investigate the involvement of HO-1 in the angiogenic activity of orexin-A. We showed that orexin-A stimulates expression and activity of HO-1 in human umbilical vein endothelial cells (HUVECs). Furthermore, we showed that inhibition of HO-1 by tin (Sn) protoporphryin-IX (SnPP) reduced orexin-A-induced angiogenesis in vivo and ex vivo. Orexin-A-stimulated endothelial tube formation and chemotactic activity were also blocked in SnPP-treated vascular endothelial cells. Orexin-A treatment increased the expression of nuclear factor erythroid-derived 2 related factor 2 (Nrf2), and antioxidant response element (ARE) luciferase activity, leading to induction of HO-1. Collectively, these findings indicate that HO-1 plays a role as an important mediator of orexin-A-induced angiogenesis, and provide new possibilities for therapeutic approaches in pathophysiological conditions associated with angiogenesis.

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“…Moreover, decrease in hippocampal expression of OX1Rs in orofacial pain situation is reported ( Raoof et al, 2015b ). In addition, orexin A anti-apoptotic and neuroprotective properties are reported in various cellular and molecular studies ( Butterick, Nixon, Billington, 2012 ; Esmaeili-Mahani, Vazifekhah, Pasban-Aliabadi, Abbasnejad, & Sheibani, 2013 ; Kitamura et al, 2010 ). Therefore, it is plausible to assume that the possible neuroprotective features of orexin A may play an effective role to prevent learning and memory impairment in the current study.…”

Section: Discussionmentioning

confidence: 99%

Research Paper: The Modulatory Role of Orexin 1 Receptor in CA1 on Orofacial Pain-induced Learning and Memory Deficits in Rats

Kooshki

Abbasnejad

Esmaeili‐Mahani

et al. 2017

BCN

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Introduction:Cognitive impairment is commonly associated with pain. The modulatory role of orexin 1 receptor (OX1R) in pain pathways as well as learning and memory processes is reported in several studies. The current study was designed to investigate the possible role of CA1-hippocampal OX1R on spatial learning and memory of rats following capsaicin-induced orofacial pain.Methods:Orofacial pain was induced by subcutaneous intra lip injection of capsaicin (100 μg). CA1 administration of orexin A and its selective antagonist (SB-334867-A) were performed 20 minutes prior to capsaicin injection. Learning and spatial memory performances were assessed by Morris Water Maze (MWM) task.Results:Capsaicin treated rats showed impairment in spatial learning and memory. In addition, pretreatment with orexin A (20 and 40 nM/rat) significantly attenuated learning and memory impairment in capsaicin-treated rats. Conversely, blockage of OX1R via SB-334867-A (40 and 80 nM/rat) significantly exaggerated learning and memory loss in capsaicin-treated rats.Conclusion:The obtained results indicated that CA1 OX1R may be involved in modulation of capsaicin –induced spatial learning and memory impairment.

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Protective effect of orexin-A on 6-hydroxydopamine-induced neurotoxicity in SH-SY5Y human dopaminergic neuroblastoma cells

Cited by 32 publications

References 39 publications

The comparison of apoptosis-related protein expressions in neurotoxin-based in vitro Parkinson s Disease models

The comparison of apoptosis-related protein expressions in neurotoxin-based in vitro Parkinson s Disease models

Involvement of Heme Oxygenase-1 in Orexin-A-induced Angiogenesis in Vascular Endothelial Cells

Research Paper: The Modulatory Role of Orexin 1 Receptor in CA1 on Orofacial Pain-induced Learning and Memory Deficits in Rats

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