Opposite effects of the gap junction blocker octanol on focal cerebral ischemia occluded for different durations
Protectants and executioners have been demonstrated to be used by gap junctions in focal cerebral ischemia. Certain researchers hypothesized that the opposite role of gap junctions may be associated with the injury extent, which has been demonstrated to be highly correlated with occlusion duration....
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| Veröffentlicht in: | Molecular medicine reports 2014-06, Vol.9 (6), p.2485-2490 |
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| creator | DING, WENTING ZHOU, LEQUAN LIU, WEI GUAN, LI LI, XIAOYING LIU, HAIMEI YAN, FUMAN XU, JINWEN ZENG, WEIYONG QIU, MIN |
| description | Protectants and executioners have been demonstrated to be used by gap junctions in focal cerebral ischemia. Certain researchers hypothesized that the opposite role of gap junctions may be associated with the injury extent, which has been demonstrated to be highly correlated with occlusion duration. In order to examine this hypothesis directly, the effects of octanol, a frequently used drug, were examined to investigate the role of gap junctions, in rats following middle cerebral artery occlusion (MCAO) for 30 min/2 h and 24 h reperfusion, respectively. Octanol significantly reduced the infarct volume following 2 h of occlusion concomitant with lower neurological deficits, whereas it enlarged the infarct volume following 30 min of occlusion. Consistently, octanol attenuated the number of transferase dUTP nick-end labeling (TUNEL) positive neurons in the hippocampal CA1 region following 2 h of occlusion, while opposite effects were observed for 30 min of occlusion. Further immunohistochemical studies demonstrated that the expression of B-cell leukemia-2 (Bcl-2, anti-apoptotic protein) was upregulated and that Bcl-2-associated X (Bax, proapoptotic protein) was downregulated following 2 h of occlusion in the octanol group compared with the ischemic group. Conversely, octanol downregulated the expression of the Bcl-2 protein concomitant with increased Bax protein following 30 min of occlusion. These results indicated that the gap junction blocker octanol can protect against ischemic injury following long-term occlusion, however, can aggravate ischemic injury following short-term occlusion. |
| doi_str_mv | 10.3892/mmr.2014.2075 |
| format | Article |
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Certain researchers hypothesized that the opposite role of gap junctions may be associated with the injury extent, which has been demonstrated to be highly correlated with occlusion duration. In order to examine this hypothesis directly, the effects of octanol, a frequently used drug, were examined to investigate the role of gap junctions, in rats following middle cerebral artery occlusion (MCAO) for 30 min/2 h and 24 h reperfusion, respectively. Octanol significantly reduced the infarct volume following 2 h of occlusion concomitant with lower neurological deficits, whereas it enlarged the infarct volume following 30 min of occlusion. Consistently, octanol attenuated the number of transferase dUTP nick-end labeling (TUNEL) positive neurons in the hippocampal CA1 region following 2 h of occlusion, while opposite effects were observed for 30 min of occlusion. Further immunohistochemical studies demonstrated that the expression of B-cell leukemia-2 (Bcl-2, anti-apoptotic protein) was upregulated and that Bcl-2-associated X (Bax, proapoptotic protein) was downregulated following 2 h of occlusion in the octanol group compared with the ischemic group. Conversely, octanol downregulated the expression of the Bcl-2 protein concomitant with increased Bax protein following 30 min of occlusion. These results indicated that the gap junction blocker octanol can protect against ischemic injury following long-term occlusion, however, can aggravate ischemic injury following short-term occlusion.</description><identifier>ISSN: 1791-2997</identifier><identifier>EISSN: 1791-3004</identifier><identifier>DOI: 10.3892/mmr.2014.2075</identifier><identifier>PMID: 24676712</identifier><language>eng</language><publisher>Greece: D.A. Spandidos</publisher><subject>Analysis ; Animals ; Apoptosis ; astrocyte ; Bax protein ; Bcl-2 protein ; bcl-2-Associated X Protein - genetics ; bcl-2-Associated X Protein - metabolism ; Brain Ischemia - metabolism ; Brain Ischemia - pathology ; Brain Ischemia - physiopathology ; Care and treatment ; Carotid arteries ; Cerebral blood flow ; Cerebral Infarction - metabolism ; Cerebral Infarction - pathology ; Cerebral Infarction - physiopathology ; Cerebral ischemia ; focal cerebral ischemia ; Gap junctions ; Gap Junctions - drug effects ; Gene Expression ; Hippocampus ; Ischemia ; Lymphocytes B ; Male ; Metabolites ; Neurological diseases ; occlusion time ; Octanol ; Octanols - administration & dosage ; Octanols - pharmacology ; Oxidative stress ; Proto-Oncogene Proteins c-bcl-2 - genetics ; Proto-Oncogene Proteins c-bcl-2 - metabolism ; Pyramidal Cells - metabolism ; Rats ; Reperfusion ; Rodents ; Roles ; Studies ; Time Factors ; Toxicity</subject><ispartof>Molecular medicine reports, 2014-06, Vol.9 (6), p.2485-2490</ispartof><rights>Copyright © 2014, Spandidos Publications</rights><rights>COPYRIGHT 2014 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2014</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c459t-b2289dd528926ddc87bfc2b167970ca177bcc6f3583b26800a30b96f54a34ab83</citedby><cites>FETCH-LOGICAL-c459t-b2289dd528926ddc87bfc2b167970ca177bcc6f3583b26800a30b96f54a34ab83</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,5556,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24676712$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>DING, WENTING</creatorcontrib><creatorcontrib>ZHOU, LEQUAN</creatorcontrib><creatorcontrib>LIU, WEI</creatorcontrib><creatorcontrib>GUAN, LI</creatorcontrib><creatorcontrib>LI, XIAOYING</creatorcontrib><creatorcontrib>LIU, HAIMEI</creatorcontrib><creatorcontrib>YAN, FUMAN</creatorcontrib><creatorcontrib>XU, JINWEN</creatorcontrib><creatorcontrib>ZENG, WEIYONG</creatorcontrib><creatorcontrib>QIU, MIN</creatorcontrib><title>Opposite effects of the gap junction blocker octanol on focal cerebral ischemia occluded for different durations</title><title>Molecular medicine reports</title><addtitle>Mol Med Rep</addtitle><description>Protectants and executioners have been demonstrated to be used by gap junctions in focal cerebral ischemia. Certain researchers hypothesized that the opposite role of gap junctions may be associated with the injury extent, which has been demonstrated to be highly correlated with occlusion duration. In order to examine this hypothesis directly, the effects of octanol, a frequently used drug, were examined to investigate the role of gap junctions, in rats following middle cerebral artery occlusion (MCAO) for 30 min/2 h and 24 h reperfusion, respectively. Octanol significantly reduced the infarct volume following 2 h of occlusion concomitant with lower neurological deficits, whereas it enlarged the infarct volume following 30 min of occlusion. Consistently, octanol attenuated the number of transferase dUTP nick-end labeling (TUNEL) positive neurons in the hippocampal CA1 region following 2 h of occlusion, while opposite effects were observed for 30 min of occlusion. Further immunohistochemical studies demonstrated that the expression of B-cell leukemia-2 (Bcl-2, anti-apoptotic protein) was upregulated and that Bcl-2-associated X (Bax, proapoptotic protein) was downregulated following 2 h of occlusion in the octanol group compared with the ischemic group. Conversely, octanol downregulated the expression of the Bcl-2 protein concomitant with increased Bax protein following 30 min of occlusion. These results indicated that the gap junction blocker octanol can protect against ischemic injury following long-term occlusion, however, can aggravate ischemic injury following short-term occlusion.</description><subject>Analysis</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>astrocyte</subject><subject>Bax protein</subject><subject>Bcl-2 protein</subject><subject>bcl-2-Associated X Protein - genetics</subject><subject>bcl-2-Associated X Protein - metabolism</subject><subject>Brain Ischemia - metabolism</subject><subject>Brain Ischemia - pathology</subject><subject>Brain Ischemia - physiopathology</subject><subject>Care and treatment</subject><subject>Carotid arteries</subject><subject>Cerebral blood flow</subject><subject>Cerebral Infarction - metabolism</subject><subject>Cerebral Infarction - pathology</subject><subject>Cerebral Infarction - physiopathology</subject><subject>Cerebral ischemia</subject><subject>focal cerebral ischemia</subject><subject>Gap junctions</subject><subject>Gap Junctions - drug effects</subject><subject>Gene Expression</subject><subject>Hippocampus</subject><subject>Ischemia</subject><subject>Lymphocytes B</subject><subject>Male</subject><subject>Metabolites</subject><subject>Neurological diseases</subject><subject>occlusion time</subject><subject>Octanol</subject><subject>Octanols - administration & dosage</subject><subject>Octanols - pharmacology</subject><subject>Oxidative stress</subject><subject>Proto-Oncogene Proteins c-bcl-2 - genetics</subject><subject>Proto-Oncogene Proteins c-bcl-2 - metabolism</subject><subject>Pyramidal Cells - metabolism</subject><subject>Rats</subject><subject>Reperfusion</subject><subject>Rodents</subject><subject>Roles</subject><subject>Studies</subject><subject>Time Factors</subject><subject>Toxicity</subject><issn>1791-2997</issn><issn>1791-3004</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNptkUtr3TAQhU1oSNK0y26LoItm41s9rNcyhD4CgWzatdAz8a0tuZK8yL-PzL1NaSmC0TB8c2aY03XvENwRIfGnec47DNHQAqcn3QXiEvUEwuHVMcdS8vPudSl7CBnFVJ5153hgnHGEL7rlfllSGasHPgRvawEpgProwYNewH6Nto4pAjMl-9NnkGzVMU2glUKyegLWZ29yS8ZiH_086obYaXXeNSADNzbR7GMFbs16kypvutOgp-LfHv_L7seXz99vvvV3919vb67vejtQWXuDsZDO0RYxc84KboLFBjEuObQacW6sZYFQQQxmAkJNoJEs0EGTQRtBLrurg-6S06_Vl6rmtqOfJh19WotCFAmBKIWkoR_-QfdpzbFtp5Ak7VZkEPgP9aAnr8YYUs3abqLqekCUSSbpNnb3H6o9165jU_RhbPW_GvpDg82plOyDWvI46_ykEFSbw6o5rDaH1eZw498fl13N7N0L_dvSBnw8AGXR0Y0ulRemKfVQ9pD1eBCUPAPmfq2H</recordid><startdate>20140601</startdate><enddate>20140601</enddate><creator>DING, WENTING</creator><creator>ZHOU, LEQUAN</creator><creator>LIU, WEI</creator><creator>GUAN, LI</creator><creator>LI, XIAOYING</creator><creator>LIU, HAIMEI</creator><creator>YAN, FUMAN</creator><creator>XU, JINWEN</creator><creator>ZENG, WEIYONG</creator><creator>QIU, MIN</creator><general>D.A. Spandidos</general><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</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>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20140601</creationdate><title>Opposite effects of the gap junction blocker octanol on focal cerebral ischemia occluded for different durations</title><author>DING, WENTING ; ZHOU, LEQUAN ; LIU, WEI ; GUAN, LI ; LI, XIAOYING ; LIU, HAIMEI ; YAN, FUMAN ; XU, JINWEN ; ZENG, WEIYONG ; QIU, MIN</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c459t-b2289dd528926ddc87bfc2b167970ca177bcc6f3583b26800a30b96f54a34ab83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Analysis</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>astrocyte</topic><topic>Bax protein</topic><topic>Bcl-2 protein</topic><topic>bcl-2-Associated X Protein - genetics</topic><topic>bcl-2-Associated X Protein - metabolism</topic><topic>Brain Ischemia - metabolism</topic><topic>Brain Ischemia - pathology</topic><topic>Brain Ischemia - physiopathology</topic><topic>Care and treatment</topic><topic>Carotid arteries</topic><topic>Cerebral blood flow</topic><topic>Cerebral Infarction - metabolism</topic><topic>Cerebral Infarction - pathology</topic><topic>Cerebral Infarction - physiopathology</topic><topic>Cerebral ischemia</topic><topic>focal cerebral ischemia</topic><topic>Gap junctions</topic><topic>Gap Junctions - drug effects</topic><topic>Gene Expression</topic><topic>Hippocampus</topic><topic>Ischemia</topic><topic>Lymphocytes B</topic><topic>Male</topic><topic>Metabolites</topic><topic>Neurological diseases</topic><topic>occlusion time</topic><topic>Octanol</topic><topic>Octanols - administration & dosage</topic><topic>Octanols - pharmacology</topic><topic>Oxidative stress</topic><topic>Proto-Oncogene Proteins c-bcl-2 - genetics</topic><topic>Proto-Oncogene Proteins c-bcl-2 - 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Academic</collection><jtitle>Molecular medicine reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>DING, WENTING</au><au>ZHOU, LEQUAN</au><au>LIU, WEI</au><au>GUAN, LI</au><au>LI, XIAOYING</au><au>LIU, HAIMEI</au><au>YAN, FUMAN</au><au>XU, JINWEN</au><au>ZENG, WEIYONG</au><au>QIU, MIN</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Opposite effects of the gap junction blocker octanol on focal cerebral ischemia occluded for different durations</atitle><jtitle>Molecular medicine reports</jtitle><addtitle>Mol Med Rep</addtitle><date>2014-06-01</date><risdate>2014</risdate><volume>9</volume><issue>6</issue><spage>2485</spage><epage>2490</epage><pages>2485-2490</pages><issn>1791-2997</issn><eissn>1791-3004</eissn><abstract>Protectants and executioners have been demonstrated to be used by gap junctions in focal cerebral ischemia. Certain researchers hypothesized that the opposite role of gap junctions may be associated with the injury extent, which has been demonstrated to be highly correlated with occlusion duration. In order to examine this hypothesis directly, the effects of octanol, a frequently used drug, were examined to investigate the role of gap junctions, in rats following middle cerebral artery occlusion (MCAO) for 30 min/2 h and 24 h reperfusion, respectively. Octanol significantly reduced the infarct volume following 2 h of occlusion concomitant with lower neurological deficits, whereas it enlarged the infarct volume following 30 min of occlusion. Consistently, octanol attenuated the number of transferase dUTP nick-end labeling (TUNEL) positive neurons in the hippocampal CA1 region following 2 h of occlusion, while opposite effects were observed for 30 min of occlusion. Further immunohistochemical studies demonstrated that the expression of B-cell leukemia-2 (Bcl-2, anti-apoptotic protein) was upregulated and that Bcl-2-associated X (Bax, proapoptotic protein) was downregulated following 2 h of occlusion in the octanol group compared with the ischemic group. Conversely, octanol downregulated the expression of the Bcl-2 protein concomitant with increased Bax protein following 30 min of occlusion. These results indicated that the gap junction blocker octanol can protect against ischemic injury following long-term occlusion, however, can aggravate ischemic injury following short-term occlusion.</abstract><cop>Greece</cop><pub>D.A. Spandidos</pub><pmid>24676712</pmid><doi>10.3892/mmr.2014.2075</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| source | Spandidos Publications Journals; MEDLINE; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Analysis Animals Apoptosis astrocyte Bax protein Bcl-2 protein bcl-2-Associated X Protein - genetics bcl-2-Associated X Protein - metabolism Brain Ischemia - metabolism Brain Ischemia - pathology Brain Ischemia - physiopathology Care and treatment Carotid arteries Cerebral blood flow Cerebral Infarction - metabolism Cerebral Infarction - pathology Cerebral Infarction - physiopathology Cerebral ischemia focal cerebral ischemia Gap junctions Gap Junctions - drug effects Gene Expression Hippocampus Ischemia Lymphocytes B Male Metabolites Neurological diseases occlusion time Octanol Octanols - administration & dosage Octanols - pharmacology Oxidative stress Proto-Oncogene Proteins c-bcl-2 - genetics Proto-Oncogene Proteins c-bcl-2 - metabolism Pyramidal Cells - metabolism Rats Reperfusion Rodents Roles Studies Time Factors Toxicity |
| title | Opposite effects of the gap junction blocker octanol on focal cerebral ischemia occluded for different durations |
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