Etanercept Attenuates Traumatic Brain Injury in Rats by Reducing Brain TNF-α Contents and by Stimulating Newly Formed Neurogenesis
It remains unclear whether etanercept penetrates directly into the contused brain and improves the outcomes of TBI by attenuating brain contents of TNF-α and/or stimulating newly formed neurogenesis. Rats that sustained TBI are immediately treated with etanercept. Acute neurological and motor injury...
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| Main Authors: | , , , , , |
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| Format: | Article |
| Language: | English |
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Wiley
2013-01-01
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| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/2013/620837 |
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| author | Chong-Un Cheong Ching-Ping Chang Chien-Ming Chao Bor-Chih Cheng Chung-Zhing Yang Chung-Ching Chio |
| author_facet | Chong-Un Cheong Ching-Ping Chang Chien-Ming Chao Bor-Chih Cheng Chung-Zhing Yang Chung-Ching Chio |
| author_sort | Chong-Un Cheong |
| collection | DOAJ |
| description | It remains unclear whether etanercept penetrates directly into the contused brain and improves the outcomes of TBI by attenuating brain contents of TNF-α and/or stimulating newly formed neurogenesis. Rats that sustained TBI are immediately treated with etanercept. Acute neurological and motor injury is assessed in all rats the day prior to and 7 days after surgery. The numbers of the colocalizations of 5-bromodeoxyuridine and doublecortin specific markers in the contused brain injury that occurred during TBI were counted by immunofluorescence staining. Enzyme immunoassay for quantitative determination of TNF-α or etanercept in brain tissues is also performed. Seven days after systemic administration of etanercept, levels of etanercept can be detected in the contused brain tissues. In addition, neurological and motor deficits, cerebral contusion, and increased brain TNF-α contents caused by TBI can be attenuated by etanercept therapy. Furthermore, the increased numbers of the colocalizations of 5-bromodeoxyuridine and doublecortin specific markers in the contused brain tissues caused by TBI can be potentiated by etanercept therapy. These findings indicate that systemically administered etanercept may penetrate directly into the contused brain tissues and may improve outcomes of TBI by reducing brain contents of TNF-α and by stimulating newly formed neurogenesis. |
| format | Article |
| id | doaj-art-500c55fa46ae45dea6b6e18f8458477f |
| institution | Kabale University |
| issn | 0962-9351 1466-1861 |
| language | English |
| publishDate | 2013-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Mediators of Inflammation |
| spelling | doaj-art-500c55fa46ae45dea6b6e18f8458477f2025-02-03T06:06:08ZengWileyMediators of Inflammation0962-93511466-18612013-01-01201310.1155/2013/620837620837Etanercept Attenuates Traumatic Brain Injury in Rats by Reducing Brain TNF-α Contents and by Stimulating Newly Formed NeurogenesisChong-Un Cheong0Ching-Ping Chang1Chien-Ming Chao2Bor-Chih Cheng3Chung-Zhing Yang4Chung-Ching Chio5Department of Intensive Care Medicine, Chi Mei Medical Center, Liouying, Tainan, TaiwanDepartment of Biotechnology, Southern Taiwan University of Science and Technology, Tainan, TaiwanDepartment of Surgery and Department of Intensive Care Medicine, Chi Mei Medical Center, Liouying, Tainan, TaiwanDepartment of Biotechnology, Southern Taiwan University of Science and Technology, Tainan, TaiwanThe Ph.D. Program for Cancer Biology and Drug Discovery, College of Medical Science and Technology, Taipei Medical University, Taipei 110, TaiwanDepartment of Surgery, Chi Mei Medical Center, Yung-Kang, Tainan, TaiwanIt remains unclear whether etanercept penetrates directly into the contused brain and improves the outcomes of TBI by attenuating brain contents of TNF-α and/or stimulating newly formed neurogenesis. Rats that sustained TBI are immediately treated with etanercept. Acute neurological and motor injury is assessed in all rats the day prior to and 7 days after surgery. The numbers of the colocalizations of 5-bromodeoxyuridine and doublecortin specific markers in the contused brain injury that occurred during TBI were counted by immunofluorescence staining. Enzyme immunoassay for quantitative determination of TNF-α or etanercept in brain tissues is also performed. Seven days after systemic administration of etanercept, levels of etanercept can be detected in the contused brain tissues. In addition, neurological and motor deficits, cerebral contusion, and increased brain TNF-α contents caused by TBI can be attenuated by etanercept therapy. Furthermore, the increased numbers of the colocalizations of 5-bromodeoxyuridine and doublecortin specific markers in the contused brain tissues caused by TBI can be potentiated by etanercept therapy. These findings indicate that systemically administered etanercept may penetrate directly into the contused brain tissues and may improve outcomes of TBI by reducing brain contents of TNF-α and by stimulating newly formed neurogenesis.http://dx.doi.org/10.1155/2013/620837 |
| spellingShingle | Chong-Un Cheong Ching-Ping Chang Chien-Ming Chao Bor-Chih Cheng Chung-Zhing Yang Chung-Ching Chio Etanercept Attenuates Traumatic Brain Injury in Rats by Reducing Brain TNF-α Contents and by Stimulating Newly Formed Neurogenesis Mediators of Inflammation |
| title | Etanercept Attenuates Traumatic Brain Injury in Rats by Reducing Brain TNF-α Contents and by Stimulating Newly Formed Neurogenesis |
| title_full | Etanercept Attenuates Traumatic Brain Injury in Rats by Reducing Brain TNF-α Contents and by Stimulating Newly Formed Neurogenesis |
| title_fullStr | Etanercept Attenuates Traumatic Brain Injury in Rats by Reducing Brain TNF-α Contents and by Stimulating Newly Formed Neurogenesis |
| title_full_unstemmed | Etanercept Attenuates Traumatic Brain Injury in Rats by Reducing Brain TNF-α Contents and by Stimulating Newly Formed Neurogenesis |
| title_short | Etanercept Attenuates Traumatic Brain Injury in Rats by Reducing Brain TNF-α Contents and by Stimulating Newly Formed Neurogenesis |
| title_sort | etanercept attenuates traumatic brain injury in rats by reducing brain tnf α contents and by stimulating newly formed neurogenesis |
| url | http://dx.doi.org/10.1155/2013/620837 |
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