Effect of Long-Term Treatment with Fimasartan on Transient Focal Ischemia in Rat Brain
Fimasartan is a newly developed angiotensin receptor blocker, which may have protective effects during myocardial infarction or atherosclerosis. In this context, we investigated the effects of long-term treatment with low-dose fimasartan on focal ischemia in rat brain. We induced focal ischemia in b...
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| creator | Ko, Sang-Bae Yoon, Byung Woo Jang, Hyunduk Kim, Dohoung Park, Hong-Kyun Jeong, Han-Gil Choi, In-Young Kim, Young-Ju Yang, Xiu-Li Kim, Chi Kyung Kim, Tae Jung |
| description | Fimasartan is a newly developed angiotensin receptor blocker, which may have protective effects during myocardial infarction or atherosclerosis. In this context, we investigated the effects of long-term treatment with low-dose fimasartan on focal ischemia in rat brain. We induced focal ischemia in brain by transient intraluminal occlusion of middle cerebral artery (MCA) and administered low-dose (0.5 mg/kg) or regular doses (1 or 3 mg/kg) of fimasartan via intravenous routes. After the administration of low-dose (0.5 mg/kg) fimasartan, blood pressure did not decrease compared to the phosphate-buffered saline- (PBS-) control with MCA occlusion (MCAO) group. The infarct volume and ischemic cell death were reduced in the low-dose fimasartan-treated group (46 ± 41 mm3 for 0.5 mg/kg and 153 ± 47 mm3 for PBS-control with MCAO; P < 0.01 ) but not in the regular-dose groups. Low-dose fimasartan treatment improved functional recovery after ischemia and significantly decreased mortality. In our study, fimasartan reduced the degradation of IκB and the formation of an inflammatory end-product, COX-2. As a result, the recruitment of inflammatory cells in the peri-infarct area decreased in fimasartan-treated group. We have demonstrated that long-term, low-dose fimasartan treatment improved outcomes after focal ischemia in the brain via a reduction of inflammation. |
| doi_str_mv | 10.1155/2015/295925 |
| format | Article |
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In this context, we investigated the effects of long-term treatment with low-dose fimasartan on focal ischemia in rat brain. We induced focal ischemia in brain by transient intraluminal occlusion of middle cerebral artery (MCA) and administered low-dose (0.5 mg/kg) or regular doses (1 or 3 mg/kg) of fimasartan via intravenous routes. After the administration of low-dose (0.5 mg/kg) fimasartan, blood pressure did not decrease compared to the phosphate-buffered saline- (PBS-) control with MCA occlusion (MCAO) group. The infarct volume and ischemic cell death were reduced in the low-dose fimasartan-treated group (46 ± 41 mm3 for 0.5 mg/kg and 153 ± 47 mm3 for PBS-control with MCAO; P < 0.01 ) but not in the regular-dose groups. Low-dose fimasartan treatment improved functional recovery after ischemia and significantly decreased mortality. In our study, fimasartan reduced the degradation of IκB and the formation of an inflammatory end-product, COX-2. As a result, the recruitment of inflammatory cells in the peri-infarct area decreased in fimasartan-treated group. We have demonstrated that long-term, low-dose fimasartan treatment improved outcomes after focal ischemia in the brain via a reduction of inflammation.</description><identifier>ISSN: 2314-6133</identifier><identifier>EISSN: 2314-6141</identifier><identifier>DOI: 10.1155/2015/295925</identifier><identifier>PMID: 26448932</identifier><language>eng</language><publisher>Cairo, Egypt: Hindawi Publishing Corporation</publisher><subject>Animals ; Antagonists (Biochemistry) ; Biomedical research ; Biphenyl Compounds - administration & dosage ; Blood pressure ; Blood Pressure - drug effects ; Brain Ischemia - drug therapy ; Brain Ischemia - metabolism ; Brain Ischemia - pathology ; Brain Ischemia - physiopathology ; Brain research ; Carotid arteries ; Cerebral ischemia ; Cyclooxygenase 2 - metabolism ; Diabetes ; Disease ; Dosage and administration ; Dose-Response Relationship, Drug ; Drug dosages ; Drug therapy ; Heart attacks ; Hospitals ; Hypertension ; Ischemia ; Male ; Mortality ; NF-kappa B - metabolism ; Patient outcomes ; Pyrimidines - administration & dosage ; Rats ; Rats, Sprague-Dawley ; Rodents ; Stroke ; Studies ; Tetrazoles - administration & dosage ; Time Factors ; Veins & arteries</subject><ispartof>BioMed research international, 2015-01, Vol.2015 (2015), p.1-9</ispartof><rights>Copyright © 2015 Chi Kyung Kim et al.</rights><rights>COPYRIGHT 2015 John Wiley & Sons, Inc.</rights><rights>Copyright © 2015 Chi Kyung Kim et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</rights><rights>Copyright © 2015 Chi Kyung Kim et al. 2015</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c528t-b1ae390ae46b460e1086b64430b1cee8b97424e0e7f9f120db851d363cc086833</citedby><cites>FETCH-LOGICAL-c528t-b1ae390ae46b460e1086b64430b1cee8b97424e0e7f9f120db851d363cc086833</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/PMC4584036/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4584036/$$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/26448932$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Xu, Gelin</contributor><creatorcontrib>Ko, Sang-Bae</creatorcontrib><creatorcontrib>Yoon, Byung Woo</creatorcontrib><creatorcontrib>Jang, Hyunduk</creatorcontrib><creatorcontrib>Kim, Dohoung</creatorcontrib><creatorcontrib>Park, Hong-Kyun</creatorcontrib><creatorcontrib>Jeong, Han-Gil</creatorcontrib><creatorcontrib>Choi, In-Young</creatorcontrib><creatorcontrib>Kim, Young-Ju</creatorcontrib><creatorcontrib>Yang, Xiu-Li</creatorcontrib><creatorcontrib>Kim, Chi Kyung</creatorcontrib><creatorcontrib>Kim, Tae Jung</creatorcontrib><title>Effect of Long-Term Treatment with Fimasartan on Transient Focal Ischemia in Rat Brain</title><title>BioMed research international</title><addtitle>Biomed Res Int</addtitle><description>Fimasartan is a newly developed angiotensin receptor blocker, which may have protective effects during myocardial infarction or atherosclerosis. In this context, we investigated the effects of long-term treatment with low-dose fimasartan on focal ischemia in rat brain. We induced focal ischemia in brain by transient intraluminal occlusion of middle cerebral artery (MCA) and administered low-dose (0.5 mg/kg) or regular doses (1 or 3 mg/kg) of fimasartan via intravenous routes. After the administration of low-dose (0.5 mg/kg) fimasartan, blood pressure did not decrease compared to the phosphate-buffered saline- (PBS-) control with MCA occlusion (MCAO) group. The infarct volume and ischemic cell death were reduced in the low-dose fimasartan-treated group (46 ± 41 mm3 for 0.5 mg/kg and 153 ± 47 mm3 for PBS-control with MCAO; P < 0.01 ) but not in the regular-dose groups. Low-dose fimasartan treatment improved functional recovery after ischemia and significantly decreased mortality. In our study, fimasartan reduced the degradation of IκB and the formation of an inflammatory end-product, COX-2. As a result, the recruitment of inflammatory cells in the peri-infarct area decreased in fimasartan-treated group. We have demonstrated that long-term, low-dose fimasartan treatment improved outcomes after focal ischemia in the brain via a reduction of inflammation.</description><subject>Animals</subject><subject>Antagonists (Biochemistry)</subject><subject>Biomedical research</subject><subject>Biphenyl Compounds - administration & dosage</subject><subject>Blood pressure</subject><subject>Blood Pressure - drug effects</subject><subject>Brain Ischemia - drug therapy</subject><subject>Brain Ischemia - metabolism</subject><subject>Brain Ischemia - pathology</subject><subject>Brain Ischemia - physiopathology</subject><subject>Brain research</subject><subject>Carotid arteries</subject><subject>Cerebral ischemia</subject><subject>Cyclooxygenase 2 - metabolism</subject><subject>Diabetes</subject><subject>Disease</subject><subject>Dosage and administration</subject><subject>Dose-Response Relationship, Drug</subject><subject>Drug dosages</subject><subject>Drug therapy</subject><subject>Heart attacks</subject><subject>Hospitals</subject><subject>Hypertension</subject><subject>Ischemia</subject><subject>Male</subject><subject>Mortality</subject><subject>NF-kappa B - metabolism</subject><subject>Patient outcomes</subject><subject>Pyrimidines - administration & dosage</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Rodents</subject><subject>Stroke</subject><subject>Studies</subject><subject>Tetrazoles - administration & dosage</subject><subject>Time Factors</subject><subject>Veins & arteries</subject><issn>2314-6133</issn><issn>2314-6141</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>RHX</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqNks1rFDEYxoMotqw9eZcBL6KM5s3XJhehlq4WFgRZvYZM9p3dlJmkJrMt_vdm2bpWT80hCTw_Hp73g5CXQN8DSPmBUaiXkYbJJ-SUcRCtAgFPj3_OT8hZKde0Hg2KGvWcnDAlhDacnZIfl32PfmpS3yxT3LQrzGOzyuimEePU3IVp2yzC6IrLk4tNilV0sYS9uEjeDc1V8Vscg2tCbL65qfmUXYgvyLPeDQXP7t8Z-b64XF18aZdfP19dnC9bL5me2g4cckMdCtUJRRGoVl3NxmkHHlF3Zi6YQIrz3vTA6LrTEtZcce8rqTmfkY8H35tdN-La11jZDfYm18j5l00u2H-VGLZ2k26tkFrQajQjb-4Ncvq5wzLZMRSPw-Aipl2xMGcMlDQgHoMCl9wwXdHX_6HXaZdj7USlQGmtFGN_qY0b0IbYpxrR703tec1Xh6U1VOrdgfI5lZKxP1YH1O53wO53wB52oNKvHjbkyP6ZeAXeHoBtiGt3Fx7nhhXB3j2ApTBC8t9aXb9E</recordid><startdate>20150101</startdate><enddate>20150101</enddate><creator>Ko, Sang-Bae</creator><creator>Yoon, Byung Woo</creator><creator>Jang, Hyunduk</creator><creator>Kim, Dohoung</creator><creator>Park, Hong-Kyun</creator><creator>Jeong, Han-Gil</creator><creator>Choi, In-Young</creator><creator>Kim, Young-Ju</creator><creator>Yang, Xiu-Li</creator><creator>Kim, Chi Kyung</creator><creator>Kim, Tae Jung</creator><general>Hindawi Publishing Corporation</general><general>John Wiley & Sons, Inc</general><general>Hindawi Limited</general><scope>ADJCN</scope><scope>AHFXO</scope><scope>RHU</scope><scope>RHW</scope><scope>RHX</scope><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>7QL</scope><scope>7QO</scope><scope>7T7</scope><scope>7TK</scope><scope>7U7</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>CWDGH</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20150101</creationdate><title>Effect of Long-Term Treatment with Fimasartan on Transient Focal Ischemia in Rat Brain</title><author>Ko, Sang-Bae ; Yoon, Byung Woo ; Jang, Hyunduk ; Kim, Dohoung ; Park, Hong-Kyun ; Jeong, Han-Gil ; Choi, In-Young ; Kim, Young-Ju ; Yang, Xiu-Li ; Kim, Chi Kyung ; Kim, Tae Jung</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c528t-b1ae390ae46b460e1086b64430b1cee8b97424e0e7f9f120db851d363cc086833</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Animals</topic><topic>Antagonists (Biochemistry)</topic><topic>Biomedical research</topic><topic>Biphenyl Compounds - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>BioMed research international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ko, Sang-Bae</au><au>Yoon, Byung Woo</au><au>Jang, Hyunduk</au><au>Kim, Dohoung</au><au>Park, Hong-Kyun</au><au>Jeong, Han-Gil</au><au>Choi, In-Young</au><au>Kim, Young-Ju</au><au>Yang, Xiu-Li</au><au>Kim, Chi Kyung</au><au>Kim, Tae Jung</au><au>Xu, Gelin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effect of Long-Term Treatment with Fimasartan on Transient Focal Ischemia in Rat Brain</atitle><jtitle>BioMed research international</jtitle><addtitle>Biomed Res Int</addtitle><date>2015-01-01</date><risdate>2015</risdate><volume>2015</volume><issue>2015</issue><spage>1</spage><epage>9</epage><pages>1-9</pages><issn>2314-6133</issn><eissn>2314-6141</eissn><abstract>Fimasartan is a newly developed angiotensin receptor blocker, which may have protective effects during myocardial infarction or atherosclerosis. In this context, we investigated the effects of long-term treatment with low-dose fimasartan on focal ischemia in rat brain. We induced focal ischemia in brain by transient intraluminal occlusion of middle cerebral artery (MCA) and administered low-dose (0.5 mg/kg) or regular doses (1 or 3 mg/kg) of fimasartan via intravenous routes. After the administration of low-dose (0.5 mg/kg) fimasartan, blood pressure did not decrease compared to the phosphate-buffered saline- (PBS-) control with MCA occlusion (MCAO) group. The infarct volume and ischemic cell death were reduced in the low-dose fimasartan-treated group (46 ± 41 mm3 for 0.5 mg/kg and 153 ± 47 mm3 for PBS-control with MCAO; P < 0.01 ) but not in the regular-dose groups. Low-dose fimasartan treatment improved functional recovery after ischemia and significantly decreased mortality. In our study, fimasartan reduced the degradation of IκB and the formation of an inflammatory end-product, COX-2. As a result, the recruitment of inflammatory cells in the peri-infarct area decreased in fimasartan-treated group. We have demonstrated that long-term, low-dose fimasartan treatment improved outcomes after focal ischemia in the brain via a reduction of inflammation.</abstract><cop>Cairo, Egypt</cop><pub>Hindawi Publishing Corporation</pub><pmid>26448932</pmid><doi>10.1155/2015/295925</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Antagonists (Biochemistry) Biomedical research Biphenyl Compounds - administration & dosage Blood pressure Blood Pressure - drug effects Brain Ischemia - drug therapy Brain Ischemia - metabolism Brain Ischemia - pathology Brain Ischemia - physiopathology Brain research Carotid arteries Cerebral ischemia Cyclooxygenase 2 - metabolism Diabetes Disease Dosage and administration Dose-Response Relationship, Drug Drug dosages Drug therapy Heart attacks Hospitals Hypertension Ischemia Male Mortality NF-kappa B - metabolism Patient outcomes Pyrimidines - administration & dosage Rats Rats, Sprague-Dawley Rodents Stroke Studies Tetrazoles - administration & dosage Time Factors Veins & arteries |
| title | Effect of Long-Term Treatment with Fimasartan on Transient Focal Ischemia in Rat Brain |
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