AccScience Publishing / ITPS / Volume 3 / Issue 1 / DOI: 10.36922/itps.v3i1.939
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RESEARCH ARTICLE

Oxytocin Promotes C6 Glial Cell Death and Aggravates Hydrogen Peroxide-induced Oxidative Stress

Ahmet Sevki Taskiran1 * Merve Ergul2
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1 Departments of Physiology, School of Medicine, Sivas Cumhuriyet University, Sivas, Turkey
2 Departments of Pharmacology, School of Pharmacy, Sivas Cumhuriyet University, Sivas, Turkey
INNOSC Theranostics and Pharmacological Sciences 2020, 3(1), 939 https://doi.org/10.36922/itps.v3i1.939
Submitted: 3 August 2020 | Accepted: 14 September 2020 | Published: 7 October 2020
© 2020 by the Authors. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution -Noncommercial 4.0 International License (CC-by the license) ( https://creativecommons.org/licenses/by-nc/4.0/ )
Abstract

Background. Recent studies have shown that oxytocin plays a vital role in neurons and glial cells. However, its effect on hydrogen peroxide (H2O2)-induced oxidative stress as well as cyclooxygenase-1 (COX-1) and COX-2 in glial cells are still unclear.
Objective. This study aims to examine the effect of oxytocin on glial cell viability, oxidative stress, COX-1, and COX-2 in C6 glial cells after exposure to H2O2.
Methods. In this study, C6 glioma cell line was used to study the effect of oxytocin on the glial cell in four cell groups. The control group was untreated. Cells in the H2O2 group were treated with 0.5 mM H2O2 for 24 h. Cells in the oxytocin group were treated with various concentrations (0.25, 0.5, 1, and 2 µg/mL) of oxytocin for 24 h. Cells in the oxytocin+H2O2 group were pre-treated with various concentrations (0.25, 0.5, 1, and 2 µg/mL) of oxytocin for 1 h before 24-h exposure to 0.5 mM H2O2. Cell viability was evaluated using XTT assay. Total antioxidant status and total oxidant status (TOS), COX-1, and COX-2 levels in the cells were measured by commercial kits.
Results. Oxytocin with various concentrations significantly decreased the viability of C6 cells after H2O2-induced oxidative stress (P < 0.01). It also significantly increased the levels of TOS, COX-1, and COX-2 in C6 cells after H2O2-induced oxidative stress (P < 0.001).
Conclusion. Oxytocin increases glial cell death after H2O2-induced oxidative damage in C6 cells, along with upregulation of COX-1 and COX-2 levels.

Keywords
Oxytocin
Oxidative stress
Cell death
Cyclooxygenase-1
Cyclooxygenase-2
C6 glioma
References
[1]

Dringen, R.; Kussmaul, L.; Hamprecht, B. Detoxification of Exogenous Hydrogen Peroxide and Organic Hydroperoxides by Cultured Astroglial Cells Assessed by Microtiter Plate Assay. Brain Res. Brain Res. Protoc., 1998, 2(3), 223–8.

[2]

Forman, H.J. Use and Abuse of Exogenous H2O2 in Studies of Signal Transduction. Free Radic. Biol. Med., 2007, 42(7), 926–32.

[3]

Halliwell, B. Oxidative Stress and Neurodegeneration: Where Are We Now? J. Neurochem., 2006, 97(6), 1634–58.

[4]

Duan, X.; Wen, Z.; Shen, H.; Shen, M.; Chen, G. Intracerebral Hemorrhage, Oxidative Stress, and Antioxidant Therapy. Oxid. Med. Cell. Longev., 2016, 2016, 1203285.

[5]

Coyle, J.T.; Puttfarcken, P. Oxidative Stress, Glutamate, and Neurodegenerative Disorders. Science, 1993, 262(5134), 689–95.

[6]

Tuppo, E.E.; Arias, H.R. The Role of Inflammation in Alzheimer’s Disease. Int. J. Biochem. Cell Biol., 2005, 37(2), 289–305.

[7]

Garden, G.A.; Campbell, B.M. Glial Biomarkers in Human Central Nervous System Disease. Glia, 2016, 64(10), 1755–71.

[8]

Verkhratsky, A.; Parpura, V.; Pekna, M.; Pekny, M.; Sofroniew, M. Glia in the Pathogenesis of Neurodegenerative Diseases. Biochem. Soc. Trans., 2014, 42(5), 1291–301.

[9]

Kocyigit, U.M.; Taşkıran, A.Ş.; Taslimi, P.; Yokuş, A.; Temel, Y.; Gulçin, İ. Inhibitory Effects of Oxytocin and Oxytocin Receptor Antagonist Atosiban on the Activities of Carbonic Anhydrase and Acetylcholinesterase Enzymes in the Liver and Kidney Tissues of Rats. J. Biochem. Mol. Toxicol., 2017, 31(11), e21972.

[10]

Algoe, S.B.; Kurtz, L.E.; Grewen, K. Oxytocin and Social Bonds: The Role of Oxytocin in Perceptions of Romantic Partners’ Bonding Behavior. Psychol. Sci., 2017, 28(12), 1763–72.

[11]

Bale, T.L.; Davis, A.M.; Auger, A.P.; Dorsa, D.M.; McCarthy, M.M. CNS Region-Specific Oxytocin Receptor Expression: Importance in Regulation of Anxiety and Sex Behavior. J. Neurosci., 2001, 21(7), 2546–52.

[12]

Cassoni, P.; Sapino, A.; Stella, A.; Fortunati, N.; Bussolati, G. Presence and Significance of Oxytocin Receptors in Human Neuroblastomas and Glial Tumors. Int. J. Cancer, 1998, 77(5), 695–700.

[13]

Cassoni, P.; Sapino, A.; Marrocco, T.; Chini, B.; Bussolati, G. Oxytocin and Oxytocin Receptors in Cancer Cells and Proliferation. J. Neuroendocrinol., 2004, 16(4), 362–4.

[14]

Lin, Y.T.; Chen, C.C.; Huang, C.C.; Nishimori, K.; Hsu, K.S. Oxytocin Stimulates Hippocampal Neurogenesis Via Oxytocin Receptor Expressed in CA3 Pyramidal Neurons. Nat. Commun., 2017, 8(1), 537.

[15]

Bakos, J.; Srancikova, A.; Havranek, T.; Bacova, Z. Molecular Mechanisms of Oxytocin Signaling at the Synaptic Connection. Neural Plast., 2018, 2018, 4864107.

[16]

Ghasemnezhad, R.; Mohammadghasemi, F.; Faghani, M.; Bahadori, M.H. Oxytocin Can Decrease Germ Cells Apoptotic Index in Testis under Acute Ischemia Reperfusion in a Rat Model. Iran. J. Reprod. Med., 2015, 13(5), 283–90.

[17]

Erel, O. A Novel Automated Direct Measurement Method for Total Antioxidant Capacity Using a New Generation, More Stable ABTS Radical Cation. Clin. Biochem., 2004, 37(4), 277–85.

[18]

Erel, O. A New Automated Colorimetric Method for Measuring Total Oxidant Status. Clin. Biochem., 2005, 38(12), 1103–11.

[19]

Yamasue, H.; Domes, G. Oxytocin and Autism Spectrum Disorders. Curr. Top. Behav. Neurosci., 2018, 35, 449–65.

[20]

Erfanparast, A.; Tamaddonfard, E.; Henareh-Chareh, F. Intra-Hippocampal Microinjection of Oxytocin Produced Antiepileptic Effect on the Pentylenetetrazol-Induced Epilepsy in Rats. Pharmacol. Rep., 2017, 69(4), 757–63.

[21]

Goodin, B.R.; Ness, T.J.; Robbins, M.T. Oxytocin-a Multifunctional Analgesic for Chronic Deep Tissue Pain. Curr. Pharm. Des., 2015, 21(7), 906–13.

[22]

Jiménez-Corral, C.; Morán-Sánchez, J.C.; Alonso-Navarro, H. Neuropeptidos en la Enfermedad de Alzheimer [Neuropeptides in Alzheimer’s Disease]. Rev. Neurol., 2006, 42(6), 354–9.

[23]

Gamal-Eltrabily, M.; Manzano-García, A. Role of Central Oxytocin and Dopamine Systems in Nociception and their Possible Interactions: Suggested Hypotheses. Rev. Neurosci., 2018, 29(4), 377–86.

[24]

Stanić, D.; Plećaš-Solarović, B.; Petrović, J.; BogavacStanojević, N.; Sopić, M.; Kotur-Stevuljević, J.; Ignjatović, S.; Pešić, V. Hydrogen Peroxide-Induced Oxidative Damage in Peripheral Blood Lymphocytes from Rats Chronically Treated with Corticosterone: The Protective Effect of Oxytocin Treatment. Chem. Biol. Interact., 2016, 256, 134–41.

[25]

Andrisic, L.; Dudzik, D.; Barbas, C.; Milkovic, L.; Grune, T.;Zarkovic, N. Short Overview on Metabolomics Approach to Study Pathophysiology of Oxidative Stress in Cancer. Redox Biol., 2018, 14, 47–58.

[26]

Cioffi, F.; Adam, R.H.I.; Broersen, K. Molecular Mechanisms and Genetics of Oxidative Stress in Alzheimer’s Disease. J. Alzheimers Dis., 2019, 72(4), 981–1017.

[27]

Elberry, A.A.; Refaie, S.M.; Kamel, M.; Ali, T.; Darwish, H.; Ashour, O. Oxytocin Ameliorates Cisplatin-Induced Nephrotoxicity in Wistar Rats. Ann. Saudi Med., 2013, 33(1), 57–62.

[28]

Karelina, K.; Stuller, K.A.; Jarrett, B.; Zhang, N.; Wells, J.; Norman, G.J.; DeVries, A.C. Oxytocin Mediates Social Neuroprotection After Cerebral Ischemia. Stroke, 2011, 42(12), 3606–11.

[29]

Breder, C.D.; Dewitt, D.; Kraig, R.P. Characterization of Inducible Cyclooxygenase in Rat Brain. J. Comp. Neurol., 1995, 355(2), 296–315.

[30]

Wouters, E.; Hudson, C.A.; McArdle, C.A.; Bernal, A.L. Central Role for Protein Kinase C in Oxytocin and Epidermal Growth Factor Stimulated Cyclooxygenase 2 Expression in Human Myometrial Cells. BMC Res. Notes, 2014, 7, 357.

[31]

Déry, M.C.; Chaudhry, P.; Leblanc, V.; Parent, S.; Fortier, A.M.; Asselin, E. Oxytocin Increases Invasive Properties of Endometrial Cancer Cells through Phosphatidylinositol 3-Kinase/AKTDependent Up-egulation of Cyclooxygenase-1, -2, and X-Linked Inhibitor of Apoptosis Protein. Biol. Reprod., 2011, 85(6), 1133–42.

Conflict of interest
The authors declare that they have no conflict of interest.
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INNOSC Theranostics and Pharmacological Sciences, Electronic ISSN: 2705-0823 Published by AccScience Publishing