Beyond the 5-HT3 receptors A role for α7nACh receptors in neuroprotective aspects of tropisetron
Accumulation of reactive oxygen species, such as hydrogen peroxide (H2O2), generated by inflammatory cells or other pathological conditions, leads to oxidative stress, which may contribute to the neuronal degeneration observed in a wide variety of neurodegenerative disorders such as Alzheimer’s dise...
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Published in | Human & experimental toxicology Vol. 34; no. 9; pp. 922 - 931 |
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Main Authors | , , , , , , , |
Format | Journal Article |
Language | English |
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London, England
SAGE Publications
01.09.2015
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Abstract | Accumulation of reactive oxygen species, such as hydrogen peroxide (H2O2), generated by inflammatory cells or other pathological conditions, leads to oxidative stress, which may contribute to the neuronal degeneration observed in a wide variety of neurodegenerative disorders such as Alzheimer’s disease. Recent investigations have described effective properties of tropisetron, such as antiphlogistic action or protection against β-amyloid induced-neuroinflammation in rats. Our data revealed that H2O2-induced cell death in rat pheochromocytoma cell line (PC12) can be inhibited by tropisetron, as defined by 3-[4, 5-dimethylthiazol-2-yl]-2, 5-diphenyl tetrazolium bromide assay, caspase 3 and caspase 12 levels. We further showed that tropisetron exerts its protective effects by upregulation of heme oxygenase-1, glutathione, catalase activity, and nuclear factor-erythroid 2 p45-related factor 2 level. Moreover, tropisetron was recently found to be a partial agonist of α7 nicotinic acetylcholine receptor (α7nAChR). The activation of α7nAChR could inhibit inflammatory and apoptotic signaling pathways in the oxidative stress conditions. In this study, selective α7nAChR antagonists (methyllycaconitine) reversed the effects of tropisetron on caspase 3 level. Our findings indicated that tropisetron can protect PC12 cells against H2O2-induced neurotoxicity through α7nAChR in vitro. |
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AbstractList | Accumulation of reactive oxygen species, such as hydrogen peroxide (H 2 O 2 ), generated by inflammatory cells or other pathological conditions, leads to oxidative stress, which may contribute to the neuronal degeneration observed in a wide variety of neurodegenerative disorders such as Alzheimer’s disease. Recent investigations have described effective properties of tropisetron, such as antiphlogistic action or protection against β-amyloid induced-neuroinflammation in rats. Our data revealed that H 2 O 2 -induced cell death in rat pheochromocytoma cell line (PC12) can be inhibited by tropisetron, as defined by 3-[4, 5-dimethylthiazol-2-yl]-2, 5-diphenyl tetrazolium bromide assay, caspase 3 and caspase 12 levels. We further showed that tropisetron exerts its protective effects by upregulation of heme oxygenase-1, glutathione, catalase activity, and nuclear factor-erythroid 2 p45-related factor 2 level. Moreover, tropisetron was recently found to be a partial agonist of α7 nicotinic acetylcholine receptor (α7nAChR). The activation of α7nAChR could inhibit inflammatory and apoptotic signaling pathways in the oxidative stress conditions. In this study, selective α7nAChR antagonists (methyllycaconitine) reversed the effects of tropisetron on caspase 3 level. Our findings indicated that tropisetron can protect PC12 cells against H 2 O 2 -induced neurotoxicity through α7nAChR in vitro. Accumulation of reactive oxygen species, such as hydrogen peroxide (H2O2), generated by inflammatory cells or other pathological conditions, leads to oxidative stress, which may contribute to the neuronal degeneration observed in a wide variety of neurodegenerative disorders such as Alzheimer’s disease. Recent investigations have described effective properties of tropisetron, such as antiphlogistic action or protection against β-amyloid induced-neuroinflammation in rats. Our data revealed that H2O2-induced cell death in rat pheochromocytoma cell line (PC12) can be inhibited by tropisetron, as defined by 3-[4, 5-dimethylthiazol-2-yl]-2, 5-diphenyl tetrazolium bromide assay, caspase 3 and caspase 12 levels. We further showed that tropisetron exerts its protective effects by upregulation of heme oxygenase-1, glutathione, catalase activity, and nuclear factor-erythroid 2 p45-related factor 2 level. Moreover, tropisetron was recently found to be a partial agonist of α7 nicotinic acetylcholine receptor (α7nAChR). The activation of α7nAChR could inhibit inflammatory and apoptotic signaling pathways in the oxidative stress conditions. In this study, selective α7nAChR antagonists (methyllycaconitine) reversed the effects of tropisetron on caspase 3 level. Our findings indicated that tropisetron can protect PC12 cells against H2O2-induced neurotoxicity through α7nAChR in vitro. |
Author | Mousavizadeh, K Khodagholi, F Dehpour, AR Khalifeh, S Mehr, SE Fakhfouri, G Kazmi, S Rahimian, R |
Author_xml | – sequence: 1 givenname: S surname: Khalifeh fullname: Khalifeh, S – sequence: 2 givenname: G surname: Fakhfouri fullname: Fakhfouri, G – sequence: 3 givenname: SE surname: Mehr fullname: Mehr, SE – sequence: 4 givenname: K surname: Mousavizadeh fullname: Mousavizadeh, K – sequence: 5 givenname: AR surname: Dehpour fullname: Dehpour, AR – sequence: 6 givenname: F surname: Khodagholi fullname: Khodagholi, F – sequence: 7 givenname: S surname: Kazmi fullname: Kazmi, S – sequence: 8 givenname: R surname: Rahimian fullname: Rahimian, R email: rahimian78@gmail.com |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/26286524$$D View this record in MEDLINE/PubMed |
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Keywords | PC12 Tropisetron α7nAChR oxidative stress 5-HT3 receptor |
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Snippet | Accumulation of reactive oxygen species, such as hydrogen peroxide (H2O2), generated by inflammatory cells or other pathological conditions, leads to oxidative... Accumulation of reactive oxygen species, such as hydrogen peroxide (H 2 O 2 ), generated by inflammatory cells or other pathological conditions, leads to... |
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SubjectTerms | alpha7 Nicotinic Acetylcholine Receptor - drug effects Animals Antioxidants - pharmacology Apoptosis - drug effects Caspases - metabolism Cell Death - drug effects Cell Survival - drug effects Cholinergic Agonists - pharmacology Hydrogen Peroxide - toxicity Indoles - pharmacology Neuroprotective Agents - pharmacology Oxidative Stress - drug effects PC12 Cells Rats Receptors, Serotonin, 5-HT3 - drug effects Serotonin 5-HT3 Receptor Antagonists - pharmacology |
Subtitle | A role for α7nACh receptors in neuroprotective aspects of tropisetron |
Title | Beyond the 5-HT3 receptors |
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