Effects of treatment with a carbon monoxide donor and an activator of heme oxygenase 1 on the nociceptive, apoptotic and/or oxidative alterations induced by persistent inflammatory pain in the central nervous system of mice
The activation of heme oxygenase 1 (HO-1)/carbon monoxide (CO) inhibits chronic inflammatory pain, but its role in the central nervous system (CNS) is not entirely known. We evaluated whether the treatment with an HO-1 inducer, cobalt protoporphyrin IX (CoPP), or a CO-releasing molecule, tricarbonyl...
| 發表在: | Brain Research Bulletin |
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| Main Authors: | , , , , |
| 格式: | Article |
| 語言: | 英语 |
| 出版: |
Elsevier
2022-10-01
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| 主題: | |
| 在線閱讀: | http://www.sciencedirect.com/science/article/pii/S0361923022001952 |
| _version_ | 1852659241611952128 |
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| author | Rafael A. Cazuza Gerard Batallé Xue Bai Christie R.A. Leite-Panissi Olga Pol |
| author_facet | Rafael A. Cazuza Gerard Batallé Xue Bai Christie R.A. Leite-Panissi Olga Pol |
| author_sort | Rafael A. Cazuza |
| collection | DOAJ |
| container_title | Brain Research Bulletin |
| description | The activation of heme oxygenase 1 (HO-1)/carbon monoxide (CO) inhibits chronic inflammatory pain, but its role in the central nervous system (CNS) is not entirely known. We evaluated whether the treatment with an HO-1 inducer, cobalt protoporphyrin IX (CoPP), or a CO-releasing molecule, tricarbonyldichlororuthenium(II)dimer (CORM-2), modulates the nociceptive, apoptotic and/or oxidative responses provoked by persistent inflammatory pain in the CNS. In C57BL/6 male mice with peripheral inflammation caused by complete Freund’s adjuvant (CFA), we assessed the effects of CORM-2 and CoPP on the expression of protein kinase B (Akt), the apoptotic protein BAX, and the antioxidant enzymes HO-1 and NADPH quinone oxidoreductase 1 (NQO1) in the periaqueductal gray matter (PAG), amygdala (AMG), ventral hippocampus (VHPC) and medial septal area (MSA). Our results showed that the increased expression of p-Akt caused by peripheral inflammation in the four analyzed brain areas was reversed by CORM-2 and CoPP therapies. Both treatments also normalized the upregulation of BAX induced by CFA on the VHPC and MSA. Oxidative stress, demonstrated with the decreased expression of HO-1 on the PAG and AMG, was normalized in CORM-2 and CoPP treated animals. CoPP also increased the expression of HO-1 on VHPC, and both treatments up-regulated the NQO1 levels on the PAG of CFA-injected animals. In conclusion, both CORM-2 and CoPP treatments inhibited the nociceptive and apoptotic responses generated by peripheral inflammation and/or potentiated the antioxidant responses in several brain areas revealing the new modulatory effects of these treatments in the CNS of animals with chronic inflammatory pain. |
| format | Article |
| id | doaj-art-967d25cfdfa64116a4caeccced07f875 |
| institution | Directory of Open Access Journals |
| issn | 1873-2747 |
| language | English |
| publishDate | 2022-10-01 |
| publisher | Elsevier |
| record_format | Article |
| spelling | doaj-art-967d25cfdfa64116a4caeccced07f8752025-08-19T21:37:30ZengElsevierBrain Research Bulletin1873-27472022-10-0118816917810.1016/j.brainresbull.2022.08.004Effects of treatment with a carbon monoxide donor and an activator of heme oxygenase 1 on the nociceptive, apoptotic and/or oxidative alterations induced by persistent inflammatory pain in the central nervous system of miceRafael A. Cazuza0Gerard Batallé1Xue Bai2Christie R.A. Leite-Panissi3Olga Pol4Department of Psychology, Faculty of Philosophy Science and Letters of Ribeirão Preto, University of São Paulo, Ribeirão Preto 14040-901, SP, BrazilGrup de Neurofarmacologia Molecular, Institut d′Investigació Biomèdica Sant Pau (IIB SANT PAU), Sant Quintí 77-79, 08041 Barcelona, Spain; Grup de Neurofarmacologia Molecular, Institut de Neurociències, Universitat Autònoma de Barcelona, 08193 Barcelona, SpainGrup de Neurofarmacologia Molecular, Institut d′Investigació Biomèdica Sant Pau (IIB SANT PAU), Sant Quintí 77-79, 08041 Barcelona, Spain; Grup de Neurofarmacologia Molecular, Institut de Neurociències, Universitat Autònoma de Barcelona, 08193 Barcelona, SpainDepartment of Psychology, Faculty of Philosophy Science and Letters of Ribeirão Preto, University of São Paulo, Ribeirão Preto 14040-901, SP, Brazil; Correspondence to: Faculdade de Filosofia, Ciências e Letras de Ribeirão Preto, Universidade de São Paulo, Ribeirão Preto 14040-901, SP, Brazil.Grup de Neurofarmacologia Molecular, Institut d′Investigació Biomèdica Sant Pau (IIB SANT PAU), Sant Quintí 77-79, 08041 Barcelona, Spain; Grup de Neurofarmacologia Molecular, Institut de Neurociències, Universitat Autònoma de Barcelona, 08193 Barcelona, Spain; Correspondence to: Institut d′Investigació Biomèdica Sant Pau & Institut de Neurociències, Universitat Autònoma de Barcelona, 08193 Barcelona, Spain.The activation of heme oxygenase 1 (HO-1)/carbon monoxide (CO) inhibits chronic inflammatory pain, but its role in the central nervous system (CNS) is not entirely known. We evaluated whether the treatment with an HO-1 inducer, cobalt protoporphyrin IX (CoPP), or a CO-releasing molecule, tricarbonyldichlororuthenium(II)dimer (CORM-2), modulates the nociceptive, apoptotic and/or oxidative responses provoked by persistent inflammatory pain in the CNS. In C57BL/6 male mice with peripheral inflammation caused by complete Freund’s adjuvant (CFA), we assessed the effects of CORM-2 and CoPP on the expression of protein kinase B (Akt), the apoptotic protein BAX, and the antioxidant enzymes HO-1 and NADPH quinone oxidoreductase 1 (NQO1) in the periaqueductal gray matter (PAG), amygdala (AMG), ventral hippocampus (VHPC) and medial septal area (MSA). Our results showed that the increased expression of p-Akt caused by peripheral inflammation in the four analyzed brain areas was reversed by CORM-2 and CoPP therapies. Both treatments also normalized the upregulation of BAX induced by CFA on the VHPC and MSA. Oxidative stress, demonstrated with the decreased expression of HO-1 on the PAG and AMG, was normalized in CORM-2 and CoPP treated animals. CoPP also increased the expression of HO-1 on VHPC, and both treatments up-regulated the NQO1 levels on the PAG of CFA-injected animals. In conclusion, both CORM-2 and CoPP treatments inhibited the nociceptive and apoptotic responses generated by peripheral inflammation and/or potentiated the antioxidant responses in several brain areas revealing the new modulatory effects of these treatments in the CNS of animals with chronic inflammatory pain.http://www.sciencedirect.com/science/article/pii/S0361923022001952ApoptosisCarbon monoxideHeme oxygenaseInflammatory painNociceptionOxidative stress |
| spellingShingle | Rafael A. Cazuza Gerard Batallé Xue Bai Christie R.A. Leite-Panissi Olga Pol Effects of treatment with a carbon monoxide donor and an activator of heme oxygenase 1 on the nociceptive, apoptotic and/or oxidative alterations induced by persistent inflammatory pain in the central nervous system of mice Apoptosis Carbon monoxide Heme oxygenase Inflammatory pain Nociception Oxidative stress |
| title | Effects of treatment with a carbon monoxide donor and an activator of heme oxygenase 1 on the nociceptive, apoptotic and/or oxidative alterations induced by persistent inflammatory pain in the central nervous system of mice |
| title_full | Effects of treatment with a carbon monoxide donor and an activator of heme oxygenase 1 on the nociceptive, apoptotic and/or oxidative alterations induced by persistent inflammatory pain in the central nervous system of mice |
| title_fullStr | Effects of treatment with a carbon monoxide donor and an activator of heme oxygenase 1 on the nociceptive, apoptotic and/or oxidative alterations induced by persistent inflammatory pain in the central nervous system of mice |
| title_full_unstemmed | Effects of treatment with a carbon monoxide donor and an activator of heme oxygenase 1 on the nociceptive, apoptotic and/or oxidative alterations induced by persistent inflammatory pain in the central nervous system of mice |
| title_short | Effects of treatment with a carbon monoxide donor and an activator of heme oxygenase 1 on the nociceptive, apoptotic and/or oxidative alterations induced by persistent inflammatory pain in the central nervous system of mice |
| title_sort | effects of treatment with a carbon monoxide donor and an activator of heme oxygenase 1 on the nociceptive apoptotic and or oxidative alterations induced by persistent inflammatory pain in the central nervous system of mice |
| topic | Apoptosis Carbon monoxide Heme oxygenase Inflammatory pain Nociception Oxidative stress |
| url | http://www.sciencedirect.com/science/article/pii/S0361923022001952 |
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