Positive Effects of Argon Inhalation After Traumatic Brain Injury in Rats
The noble gas argon is one of the most promising neuroprotective agents for hypoxic-reperfusion injuries of the brain. However, its effect on traumatic injuries has been insufficiently studied. The aim of this study was to analyze the effect of the triple inhalation of the argon-oxygen mixture Ar 70...
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creator | Antonova, Viktoriya V Silachev, Denis N Plotnikov, Egor Y Pevzner, Irina B Ivanov, Mikhail E Boeva, Ekaterina A Kalabushev, Sergey N Yadgarov, Mikhail Ya Cherpakov, Rostislav A Grebenchikov, Oleg A Kuzovlev, Artem N |
description | The noble gas argon is one of the most promising neuroprotective agents for hypoxic-reperfusion injuries of the brain. However, its effect on traumatic injuries has been insufficiently studied. The aim of this study was to analyze the effect of the triple inhalation of the argon-oxygen mixture Ar 70%/O
30% on physical and neurological recovery and the degree of brain damage after traumatic brain injury and to investigate the possible molecular mechanisms of the neuroprotective effect. The experiments were performed in male Wistar rats. A controlled brain injury model was used to investigate the effects of argon treatment and the underlying molecular mechanisms. The results of the study showed that animals with craniocerebral injuries that were treated with argon inhalation exhibited better physical recovery rates, better neurological status, and less brain damage. Argon treatment significantly reduced the expression of the proinflammatory markers TNFα and CD68 caused by TBI, increased the expression of phosphorylated protein kinase B (pAKT), and promoted the expression of the transcription factor Nrf2 in intact animals. Treatment with an argon-oxygen breathing mixture after traumatic brain injury has a neuroprotective effect by suppressing the inflammatory response and activating the antioxidant and anti-ischemic system. |
doi_str_mv | 10.3390/ijms252312673 |
format | Article |
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30% on physical and neurological recovery and the degree of brain damage after traumatic brain injury and to investigate the possible molecular mechanisms of the neuroprotective effect. The experiments were performed in male Wistar rats. A controlled brain injury model was used to investigate the effects of argon treatment and the underlying molecular mechanisms. The results of the study showed that animals with craniocerebral injuries that were treated with argon inhalation exhibited better physical recovery rates, better neurological status, and less brain damage. Argon treatment significantly reduced the expression of the proinflammatory markers TNFα and CD68 caused by TBI, increased the expression of phosphorylated protein kinase B (pAKT), and promoted the expression of the transcription factor Nrf2 in intact animals. Treatment with an argon-oxygen breathing mixture after traumatic brain injury has a neuroprotective effect by suppressing the inflammatory response and activating the antioxidant and anti-ischemic system.</description><identifier>ISSN: 1422-0067</identifier><identifier>ISSN: 1661-6596</identifier><identifier>EISSN: 1422-0067</identifier><identifier>DOI: 10.3390/ijms252312673</identifier><identifier>PMID: 39684384</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Administration, Inhalation ; Animals ; Antioxidants ; Argon ; Argon - pharmacology ; Brain ; Brain Injuries, Traumatic - drug therapy ; Brain Injuries, Traumatic - metabolism ; Brain Injuries, Traumatic - pathology ; Cysts ; Disease Models, Animal ; Health aspects ; Hypoxia ; Injuries ; Investigations ; Ischemia ; Laboratory animals ; Magnetic resonance imaging ; Male ; Neuroprotective Agents - administration & dosage ; Neuroprotective Agents - pharmacology ; Neuroprotective Agents - therapeutic use ; NF-E2-Related Factor 2 - metabolism ; Pathogenesis ; Postoperative period ; Proto-Oncogene Proteins c-akt - metabolism ; Rats ; Rats, Wistar ; Transcription factors ; Traumatic brain injury ; Tumor Necrosis Factor-alpha - metabolism</subject><ispartof>International journal of molecular sciences, 2024-12, Vol.25 (23), p.12673</ispartof><rights>COPYRIGHT 2024 MDPI AG</rights><rights>2024 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c313t-8ed3b43a402c2bf0738ed97a24f4f6825fa7e79717aea947b6ecb6ff15f439b53</cites><orcidid>0000-0002-0819-7886 ; 0000-0001-7017-7897 ; 0000-0001-5048-1234 ; 0000-0003-0581-9755 ; 0000-0003-3792-1682 ; 0000-0002-5930-0118 ; 0000-0003-2838-3704 ; 0000-0002-5010-3919</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,778,782,27907,27908</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/39684384$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Antonova, Viktoriya V</creatorcontrib><creatorcontrib>Silachev, Denis N</creatorcontrib><creatorcontrib>Plotnikov, Egor Y</creatorcontrib><creatorcontrib>Pevzner, Irina B</creatorcontrib><creatorcontrib>Ivanov, Mikhail E</creatorcontrib><creatorcontrib>Boeva, Ekaterina A</creatorcontrib><creatorcontrib>Kalabushev, Sergey N</creatorcontrib><creatorcontrib>Yadgarov, Mikhail Ya</creatorcontrib><creatorcontrib>Cherpakov, Rostislav A</creatorcontrib><creatorcontrib>Grebenchikov, Oleg A</creatorcontrib><creatorcontrib>Kuzovlev, Artem N</creatorcontrib><title>Positive Effects of Argon Inhalation After Traumatic Brain Injury in Rats</title><title>International journal of molecular sciences</title><addtitle>Int J Mol Sci</addtitle><description>The noble gas argon is one of the most promising neuroprotective agents for hypoxic-reperfusion injuries of the brain. However, its effect on traumatic injuries has been insufficiently studied. The aim of this study was to analyze the effect of the triple inhalation of the argon-oxygen mixture Ar 70%/O
30% on physical and neurological recovery and the degree of brain damage after traumatic brain injury and to investigate the possible molecular mechanisms of the neuroprotective effect. The experiments were performed in male Wistar rats. A controlled brain injury model was used to investigate the effects of argon treatment and the underlying molecular mechanisms. The results of the study showed that animals with craniocerebral injuries that were treated with argon inhalation exhibited better physical recovery rates, better neurological status, and less brain damage. Argon treatment significantly reduced the expression of the proinflammatory markers TNFα and CD68 caused by TBI, increased the expression of phosphorylated protein kinase B (pAKT), and promoted the expression of the transcription factor Nrf2 in intact animals. Treatment with an argon-oxygen breathing mixture after traumatic brain injury has a neuroprotective effect by suppressing the inflammatory response and activating the antioxidant and anti-ischemic system.</description><subject>Administration, Inhalation</subject><subject>Animals</subject><subject>Antioxidants</subject><subject>Argon</subject><subject>Argon - pharmacology</subject><subject>Brain</subject><subject>Brain Injuries, Traumatic - drug therapy</subject><subject>Brain Injuries, Traumatic - metabolism</subject><subject>Brain Injuries, Traumatic - pathology</subject><subject>Cysts</subject><subject>Disease Models, Animal</subject><subject>Health aspects</subject><subject>Hypoxia</subject><subject>Injuries</subject><subject>Investigations</subject><subject>Ischemia</subject><subject>Laboratory animals</subject><subject>Magnetic resonance imaging</subject><subject>Male</subject><subject>Neuroprotective Agents - administration & dosage</subject><subject>Neuroprotective Agents - pharmacology</subject><subject>Neuroprotective Agents - therapeutic use</subject><subject>NF-E2-Related Factor 2 - metabolism</subject><subject>Pathogenesis</subject><subject>Postoperative period</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Transcription factors</subject><subject>Traumatic brain injury</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><issn>1422-0067</issn><issn>1661-6596</issn><issn>1422-0067</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNptkUtLxDAUhYMojq-lWym4cdMxyU2bZjkOPgYGFNF1STOJprSNJq0w_96U8Y3cxT0cvns5cBA6JngKIPC5rdtAMwqE5hy20B5hlKYY53z7h56g_RBqjCnQTOyiCYi8YFCwPbS4c8H29k0nl8Zo1YfEmWTmn1yXLLpn2cjeRjkzvfbJg5dDGw2VXHhpR6Ae_DqJ6l724RDtGNkEffSxD9Dj1eXD_CZd3l4v5rNlqoBAnxZ6BRUDyTBVtDKYQ3QEl5QZZvKCZkZyzQUnXGopGK9yrarcGJIZBqLK4ACdbf6-ePc66NCXrQ1KN43stBtCCYTlguRMkIie_kFrN_guphspRoQocPFNPclGl7YzrvdSjU_LWRGZjDCASE3_oeKsdGuV67Sx0f91kG4OlHcheG3KF29b6dclweVYXfmrusiffIQdqlavvujPruAdUOiRig</recordid><startdate>20241201</startdate><enddate>20241201</enddate><creator>Antonova, Viktoriya V</creator><creator>Silachev, Denis N</creator><creator>Plotnikov, Egor Y</creator><creator>Pevzner, Irina B</creator><creator>Ivanov, Mikhail E</creator><creator>Boeva, Ekaterina A</creator><creator>Kalabushev, Sergey N</creator><creator>Yadgarov, Mikhail Ya</creator><creator>Cherpakov, Rostislav A</creator><creator>Grebenchikov, Oleg A</creator><creator>Kuzovlev, Artem N</creator><general>MDPI AG</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-0819-7886</orcidid><orcidid>https://orcid.org/0000-0001-7017-7897</orcidid><orcidid>https://orcid.org/0000-0001-5048-1234</orcidid><orcidid>https://orcid.org/0000-0003-0581-9755</orcidid><orcidid>https://orcid.org/0000-0003-3792-1682</orcidid><orcidid>https://orcid.org/0000-0002-5930-0118</orcidid><orcidid>https://orcid.org/0000-0003-2838-3704</orcidid><orcidid>https://orcid.org/0000-0002-5010-3919</orcidid></search><sort><creationdate>20241201</creationdate><title>Positive Effects of Argon Inhalation After Traumatic Brain Injury in Rats</title><author>Antonova, Viktoriya V ; Silachev, Denis N ; Plotnikov, Egor Y ; Pevzner, Irina B ; Ivanov, Mikhail E ; Boeva, Ekaterina A ; Kalabushev, Sergey N ; Yadgarov, Mikhail Ya ; Cherpakov, Rostislav A ; Grebenchikov, Oleg A ; Kuzovlev, Artem N</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c313t-8ed3b43a402c2bf0738ed97a24f4f6825fa7e79717aea947b6ecb6ff15f439b53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Administration, Inhalation</topic><topic>Animals</topic><topic>Antioxidants</topic><topic>Argon</topic><topic>Argon - 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Academic</collection><jtitle>International journal of molecular sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Antonova, Viktoriya V</au><au>Silachev, Denis N</au><au>Plotnikov, Egor Y</au><au>Pevzner, Irina B</au><au>Ivanov, Mikhail E</au><au>Boeva, Ekaterina A</au><au>Kalabushev, Sergey N</au><au>Yadgarov, Mikhail Ya</au><au>Cherpakov, Rostislav A</au><au>Grebenchikov, Oleg A</au><au>Kuzovlev, Artem N</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Positive Effects of Argon Inhalation After Traumatic Brain Injury in Rats</atitle><jtitle>International journal of molecular sciences</jtitle><addtitle>Int J Mol Sci</addtitle><date>2024-12-01</date><risdate>2024</risdate><volume>25</volume><issue>23</issue><spage>12673</spage><pages>12673-</pages><issn>1422-0067</issn><issn>1661-6596</issn><eissn>1422-0067</eissn><abstract>The noble gas argon is one of the most promising neuroprotective agents for hypoxic-reperfusion injuries of the brain. However, its effect on traumatic injuries has been insufficiently studied. The aim of this study was to analyze the effect of the triple inhalation of the argon-oxygen mixture Ar 70%/O
30% on physical and neurological recovery and the degree of brain damage after traumatic brain injury and to investigate the possible molecular mechanisms of the neuroprotective effect. The experiments were performed in male Wistar rats. A controlled brain injury model was used to investigate the effects of argon treatment and the underlying molecular mechanisms. The results of the study showed that animals with craniocerebral injuries that were treated with argon inhalation exhibited better physical recovery rates, better neurological status, and less brain damage. Argon treatment significantly reduced the expression of the proinflammatory markers TNFα and CD68 caused by TBI, increased the expression of phosphorylated protein kinase B (pAKT), and promoted the expression of the transcription factor Nrf2 in intact animals. Treatment with an argon-oxygen breathing mixture after traumatic brain injury has a neuroprotective effect by suppressing the inflammatory response and activating the antioxidant and anti-ischemic system.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>39684384</pmid><doi>10.3390/ijms252312673</doi><orcidid>https://orcid.org/0000-0002-0819-7886</orcidid><orcidid>https://orcid.org/0000-0001-7017-7897</orcidid><orcidid>https://orcid.org/0000-0001-5048-1234</orcidid><orcidid>https://orcid.org/0000-0003-0581-9755</orcidid><orcidid>https://orcid.org/0000-0003-3792-1682</orcidid><orcidid>https://orcid.org/0000-0002-5930-0118</orcidid><orcidid>https://orcid.org/0000-0003-2838-3704</orcidid><orcidid>https://orcid.org/0000-0002-5010-3919</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Administration, Inhalation Animals Antioxidants Argon Argon - pharmacology Brain Brain Injuries, Traumatic - drug therapy Brain Injuries, Traumatic - metabolism Brain Injuries, Traumatic - pathology Cysts Disease Models, Animal Health aspects Hypoxia Injuries Investigations Ischemia Laboratory animals Magnetic resonance imaging Male Neuroprotective Agents - administration & dosage Neuroprotective Agents - pharmacology Neuroprotective Agents - therapeutic use NF-E2-Related Factor 2 - metabolism Pathogenesis Postoperative period Proto-Oncogene Proteins c-akt - metabolism Rats Rats, Wistar Transcription factors Traumatic brain injury Tumor Necrosis Factor-alpha - metabolism |
title | Positive Effects of Argon Inhalation After Traumatic Brain Injury in Rats |
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