Progesterone protects blood-brain barrier function and improves neurological outcome following traumatic brain injury in rats
Inflammatory responses are associated with blood-brain barrier (BBB) dysfunction and neurological deficits following traumatic brain injury (TBI). The aim of the present study was to investigate the effects of progesterone on the expression of the inflammatory mediators prostaglandin E2 (PGE2), cycl...
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Veröffentlicht in: | Experimental and therapeutic medicine 2014-09, Vol.8 (3), p.1010-1014 |
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description | Inflammatory responses are associated with blood-brain barrier (BBB) dysfunction and neurological deficits following traumatic brain injury (TBI). The aim of the present study was to investigate the effects of progesterone on the expression of the inflammatory mediators prostaglandin E2 (PGE2), cyclooxygenase-2 (COX-2), nuclear factor κB (NF-κB) and tumor necrosis factor-α (TNF-α) in the brain, BBB permeability, cerebral edema and neurological outcome, as well as to explore the mechanism of its neuroprotective effect. In this study, male rats were randomly divided into three groups: a sham-operated group (SHAM), a TBI group (TBI) and a progesterone treatment group (TBI-PROG). The TBI model was established using a modified Feeney's weight-dropping method. Brain samples were extracted 24 h following injury. The expression levels of COX-2 and NF-κB were examined using immunohistochemistry, whilst the expression levels of PGE2 and TNF-α were detected by enzyme-linked immunosorbent assay. BBB permeability was analyzed using Evans blue and cerebral edema was determined using the dry-wet method. The neurological outcome was evaluated using the modified neurological severity score test. The results revealed that progesterone treatment significantly reduced post-injury inflammatory response, brain edema and Evans blue dye extravasation, and improved neurological scores compared with those in the TBI group. In conclusion, the inhibition of inflammation may be an important mechanism by which progesterone protects the BBB and improves neurological outcome. |
doi_str_mv | 10.3892/etm.2014.1840 |
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The aim of the present study was to investigate the effects of progesterone on the expression of the inflammatory mediators prostaglandin E2 (PGE2), cyclooxygenase-2 (COX-2), nuclear factor κB (NF-κB) and tumor necrosis factor-α (TNF-α) in the brain, BBB permeability, cerebral edema and neurological outcome, as well as to explore the mechanism of its neuroprotective effect. In this study, male rats were randomly divided into three groups: a sham-operated group (SHAM), a TBI group (TBI) and a progesterone treatment group (TBI-PROG). The TBI model was established using a modified Feeney's weight-dropping method. Brain samples were extracted 24 h following injury. The expression levels of COX-2 and NF-κB were examined using immunohistochemistry, whilst the expression levels of PGE2 and TNF-α were detected by enzyme-linked immunosorbent assay. BBB permeability was analyzed using Evans blue and cerebral edema was determined using the dry-wet method. The neurological outcome was evaluated using the modified neurological severity score test. The results revealed that progesterone treatment significantly reduced post-injury inflammatory response, brain edema and Evans blue dye extravasation, and improved neurological scores compared with those in the TBI group. In conclusion, the inhibition of inflammation may be an important mechanism by which progesterone protects the BBB and improves neurological outcome.</description><identifier>ISSN: 1792-0981</identifier><identifier>EISSN: 1792-1015</identifier><identifier>DOI: 10.3892/etm.2014.1840</identifier><identifier>PMID: 25120639</identifier><language>eng</language><publisher>Greece: D.A. Spandidos</publisher><subject>Blood-brain barrier ; Brain ; Dosage and administration ; Edema ; Inflammation ; Injuries ; Lipid peroxidation ; Lipids ; Metabolism ; neurological function ; Permeability ; Physiological aspects ; Progesterone ; Rodents ; Studies ; Trauma ; Traumatic brain injury ; Tumor necrosis factor-TNF</subject><ispartof>Experimental and therapeutic medicine, 2014-09, Vol.8 (3), p.1010-1014</ispartof><rights>Copyright © 2014, Spandidos Publications</rights><rights>COPYRIGHT 2014 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2014</rights><rights>Copyright © 2014, Spandidos Publications 2014</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c580t-d2d8893005682f64a908b0baf05506392e8f886e80981ca64e4640ed0fb848c43</citedby><cites>FETCH-LOGICAL-c580t-d2d8893005682f64a908b0baf05506392e8f886e80981ca64e4640ed0fb848c43</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4113529/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4113529/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25120639$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>SI, DAOWEN</creatorcontrib><creatorcontrib>LI, JUAN</creatorcontrib><creatorcontrib>LIU, JIANG</creatorcontrib><creatorcontrib>WANG, XIAOYIN</creatorcontrib><creatorcontrib>WEI, ZIFENG</creatorcontrib><creatorcontrib>TIAN, QINGYOU</creatorcontrib><creatorcontrib>WANG, HAITAO</creatorcontrib><creatorcontrib>LIU, GANG</creatorcontrib><title>Progesterone protects blood-brain barrier function and improves neurological outcome following traumatic brain injury in rats</title><title>Experimental and therapeutic medicine</title><addtitle>Exp Ther Med</addtitle><description>Inflammatory responses are associated with blood-brain barrier (BBB) dysfunction and neurological deficits following traumatic brain injury (TBI). The aim of the present study was to investigate the effects of progesterone on the expression of the inflammatory mediators prostaglandin E2 (PGE2), cyclooxygenase-2 (COX-2), nuclear factor κB (NF-κB) and tumor necrosis factor-α (TNF-α) in the brain, BBB permeability, cerebral edema and neurological outcome, as well as to explore the mechanism of its neuroprotective effect. In this study, male rats were randomly divided into three groups: a sham-operated group (SHAM), a TBI group (TBI) and a progesterone treatment group (TBI-PROG). The TBI model was established using a modified Feeney's weight-dropping method. Brain samples were extracted 24 h following injury. The expression levels of COX-2 and NF-κB were examined using immunohistochemistry, whilst the expression levels of PGE2 and TNF-α were detected by enzyme-linked immunosorbent assay. BBB permeability was analyzed using Evans blue and cerebral edema was determined using the dry-wet method. The neurological outcome was evaluated using the modified neurological severity score test. The results revealed that progesterone treatment significantly reduced post-injury inflammatory response, brain edema and Evans blue dye extravasation, and improved neurological scores compared with those in the TBI group. In conclusion, the inhibition of inflammation may be an important mechanism by which progesterone protects the BBB and improves neurological outcome.</description><subject>Blood-brain barrier</subject><subject>Brain</subject><subject>Dosage and administration</subject><subject>Edema</subject><subject>Inflammation</subject><subject>Injuries</subject><subject>Lipid peroxidation</subject><subject>Lipids</subject><subject>Metabolism</subject><subject>neurological function</subject><subject>Permeability</subject><subject>Physiological aspects</subject><subject>Progesterone</subject><subject>Rodents</subject><subject>Studies</subject><subject>Trauma</subject><subject>Traumatic brain injury</subject><subject>Tumor necrosis factor-TNF</subject><issn>1792-0981</issn><issn>1792-1015</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNptkkuPFCEUhStG40zGWbo1JC50Uy2vKm9tTCYTX8kkutA1oahbLR0KWqDGzML_LqTb1jHCAgIfBw73NM1TRjcCBv4K87LhlMkNA0kfNOfs9cBbRln38DinA7Cz5jKlHS2t6xlA97g54x3jtBfDefPzcwxbTBlj8Ej2MWQ0OZHRhTC1Y9TWk1HHaDGSefUm2-CJ9hOxS2FvMRGPawwubK3RjoQ1m7AgmYNz4Yf1W5KjXhedrSEHMet3a7wrA4k6pyfNo1m7hJfH8aL5-u7tl-sP7c2n9x-vr25a0wHN7cQngEFUA8DnXuqBwkhHPdOuqzY4wgzQI1S7RvcSZS8pTnQeQYKR4qJ5c9Ddr-OCk0Ff3uXUPtpFxzsVtFX3d7z9prbhVknGRMeHIvDyKBDD97X8l1psMuic9hjWpBjwvhsAREWf_4Puwhp9safYIEpxoDzuD7XVDpX1cyj3miqqrgRIXpxA1dr8hyp9wsWaUrHZlvV7B9rDARNDShHnk0dGVY2MKpFRNTKqRqbwz_7-mBP9OyAFeHEA0r6U3U4hnZii1FJoqaiJo-IXY3XKvw</recordid><startdate>20140901</startdate><enddate>20140901</enddate><creator>SI, DAOWEN</creator><creator>LI, JUAN</creator><creator>LIU, JIANG</creator><creator>WANG, XIAOYIN</creator><creator>WEI, ZIFENG</creator><creator>TIAN, QINGYOU</creator><creator>WANG, HAITAO</creator><creator>LIU, GANG</creator><general>D.A. 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The aim of the present study was to investigate the effects of progesterone on the expression of the inflammatory mediators prostaglandin E2 (PGE2), cyclooxygenase-2 (COX-2), nuclear factor κB (NF-κB) and tumor necrosis factor-α (TNF-α) in the brain, BBB permeability, cerebral edema and neurological outcome, as well as to explore the mechanism of its neuroprotective effect. In this study, male rats were randomly divided into three groups: a sham-operated group (SHAM), a TBI group (TBI) and a progesterone treatment group (TBI-PROG). The TBI model was established using a modified Feeney's weight-dropping method. Brain samples were extracted 24 h following injury. The expression levels of COX-2 and NF-κB were examined using immunohistochemistry, whilst the expression levels of PGE2 and TNF-α were detected by enzyme-linked immunosorbent assay. BBB permeability was analyzed using Evans blue and cerebral edema was determined using the dry-wet method. The neurological outcome was evaluated using the modified neurological severity score test. The results revealed that progesterone treatment significantly reduced post-injury inflammatory response, brain edema and Evans blue dye extravasation, and improved neurological scores compared with those in the TBI group. In conclusion, the inhibition of inflammation may be an important mechanism by which progesterone protects the BBB and improves neurological outcome.</abstract><cop>Greece</cop><pub>D.A. Spandidos</pub><pmid>25120639</pmid><doi>10.3892/etm.2014.1840</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Blood-brain barrier Brain Dosage and administration Edema Inflammation Injuries Lipid peroxidation Lipids Metabolism neurological function Permeability Physiological aspects Progesterone Rodents Studies Trauma Traumatic brain injury Tumor necrosis factor-TNF |
title | Progesterone protects blood-brain barrier function and improves neurological outcome following traumatic brain injury in rats |
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