The role of heat shock protein 70 in the protective effect of YC-1 on heat stroke rats
Heat stroke is a life-threatening illness characterized by an elevated core body temperature. Despite adequate lowering of the body temperature and support treatment of multiple organ-system function, heat stroke is often fatal. 3-(5′-Hydoxymethyl-2′-furyl)-1-benzyl-indazol (YC-1) been identified as...
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| Veröffentlicht in: | European journal of pharmacology 2013-01, Vol.699 (1-3), p.67-73 |
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| container_title | European journal of pharmacology |
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| creator | Lam, Kwok-Keung Cheng, Pao-Yun Lee, Yen-Mei Liu, Yu-Pei Ding, Cheng Liu, Won-Hsiung Yen, Mao-Hsiung |
| description | Heat stroke is a life-threatening illness characterized by an elevated core body temperature. Despite adequate lowering of the body temperature and support treatment of multiple organ-system function, heat stroke is often fatal. 3-(5′-Hydoxymethyl-2′-furyl)-1-benzyl-indazol (YC-1) been identified as an activator of soluble guanylate cyclase. To evaluate whether YC-1 protects multiple organ dysfunctions and improves survival during heat stroke and its mechanism. Male Sprague-Dawley rats untreated or treated with either YC-1 or quercetin (heat shock protein (Hsp) 70 inhibitor) were exposures to heat as a model of heat stroke. The mean arterial pressure (MAP), heart rate, rectal temperature (Tco), survival time, and plasma biochemical data, intracellular Hsp70 and heat shock factor-1 expression were measured. The value of MAP, heart rate and Tco of untreated heat stroke (HS) group were all significantly lower than that of normothermal (NT) group. Biochemical markers evidenced that liver and kidney injuries of HS group were significantly higher than that of NT groups. YC-1 (20mg/kg) pretreatment with heat stroke (YC-1+HS) group, the MAP and heart rate were return to normal, and the biochemical markers were all significantly recovered to normal. The survival time of HS group, NT group and YC-1+HS group were 21, 480, and 445min, respectively. The expression of Hsp70 and HSF-1 in liver and renal of YC-1+HS group was significantly higher than that of HS group. All of the protective effects of YC-1 were all significantly suppressed when pretreated with quercetin (400mg/kg). Results indicate that YC-1 may improve survival due to induce Hsp70 overexpression. |
| doi_str_mv | 10.1016/j.ejphar.2012.11.044 |
| format | Article |
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Despite adequate lowering of the body temperature and support treatment of multiple organ-system function, heat stroke is often fatal. 3-(5′-Hydoxymethyl-2′-furyl)-1-benzyl-indazol (YC-1) been identified as an activator of soluble guanylate cyclase. To evaluate whether YC-1 protects multiple organ dysfunctions and improves survival during heat stroke and its mechanism. Male Sprague-Dawley rats untreated or treated with either YC-1 or quercetin (heat shock protein (Hsp) 70 inhibitor) were exposures to heat as a model of heat stroke. The mean arterial pressure (MAP), heart rate, rectal temperature (Tco), survival time, and plasma biochemical data, intracellular Hsp70 and heat shock factor-1 expression were measured. The value of MAP, heart rate and Tco of untreated heat stroke (HS) group were all significantly lower than that of normothermal (NT) group. Biochemical markers evidenced that liver and kidney injuries of HS group were significantly higher than that of NT groups. YC-1 (20mg/kg) pretreatment with heat stroke (YC-1+HS) group, the MAP and heart rate were return to normal, and the biochemical markers were all significantly recovered to normal. The survival time of HS group, NT group and YC-1+HS group were 21, 480, and 445min, respectively. The expression of Hsp70 and HSF-1 in liver and renal of YC-1+HS group was significantly higher than that of HS group. All of the protective effects of YC-1 were all significantly suppressed when pretreated with quercetin (400mg/kg). Results indicate that YC-1 may improve survival due to induce Hsp70 overexpression.</description><identifier>ISSN: 0014-2999</identifier><identifier>EISSN: 1879-0712</identifier><identifier>DOI: 10.1016/j.ejphar.2012.11.044</identifier><identifier>PMID: 23219797</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>Animals ; Arterial Pressure - drug effects ; biomarkers ; body temperature ; Disease Models, Animal ; DNA-Binding Proteins - genetics ; Enzyme Activators - pharmacology ; Gene Expression Regulation - drug effects ; guanylate cyclase ; heart rate ; Heart Rate - drug effects ; Heat shock factor-1 ; Heat shock protein ; Heat shock response ; Heat Shock Transcription Factors ; heat stress ; Heat stroke ; Heat Stroke - drug therapy ; Heat Stroke - physiopathology ; heat-shock protein 70 ; HSP70 Heat-Shock Proteins - metabolism ; Indazoles - pharmacology ; Kidney - drug effects ; Kidney - pathology ; kidneys ; liver ; Liver - drug effects ; Liver - pathology ; Male ; pharmacology ; protective effect ; quercetin ; Quercetin - pharmacology ; Rats ; Rats, Sprague-Dawley ; Survival Rate ; Transcription Factors - genetics ; YC-1</subject><ispartof>European journal of pharmacology, 2013-01, Vol.699 (1-3), p.67-73</ispartof><rights>2012 Elsevier B.V.</rights><rights>Copyright © 2012 Elsevier B.V. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c452t-1ad66f96c0c645411e8d0693809245be6bcb9f8e764acd10e55331143df7acd83</citedby><cites>FETCH-LOGICAL-c452t-1ad66f96c0c645411e8d0693809245be6bcb9f8e764acd10e55331143df7acd83</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.ejphar.2012.11.044$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23219797$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lam, Kwok-Keung</creatorcontrib><creatorcontrib>Cheng, Pao-Yun</creatorcontrib><creatorcontrib>Lee, Yen-Mei</creatorcontrib><creatorcontrib>Liu, Yu-Pei</creatorcontrib><creatorcontrib>Ding, Cheng</creatorcontrib><creatorcontrib>Liu, Won-Hsiung</creatorcontrib><creatorcontrib>Yen, Mao-Hsiung</creatorcontrib><title>The role of heat shock protein 70 in the protective effect of YC-1 on heat stroke rats</title><title>European journal of pharmacology</title><addtitle>Eur J Pharmacol</addtitle><description>Heat stroke is a life-threatening illness characterized by an elevated core body temperature. Despite adequate lowering of the body temperature and support treatment of multiple organ-system function, heat stroke is often fatal. 3-(5′-Hydoxymethyl-2′-furyl)-1-benzyl-indazol (YC-1) been identified as an activator of soluble guanylate cyclase. To evaluate whether YC-1 protects multiple organ dysfunctions and improves survival during heat stroke and its mechanism. Male Sprague-Dawley rats untreated or treated with either YC-1 or quercetin (heat shock protein (Hsp) 70 inhibitor) were exposures to heat as a model of heat stroke. The mean arterial pressure (MAP), heart rate, rectal temperature (Tco), survival time, and plasma biochemical data, intracellular Hsp70 and heat shock factor-1 expression were measured. The value of MAP, heart rate and Tco of untreated heat stroke (HS) group were all significantly lower than that of normothermal (NT) group. Biochemical markers evidenced that liver and kidney injuries of HS group were significantly higher than that of NT groups. YC-1 (20mg/kg) pretreatment with heat stroke (YC-1+HS) group, the MAP and heart rate were return to normal, and the biochemical markers were all significantly recovered to normal. The survival time of HS group, NT group and YC-1+HS group were 21, 480, and 445min, respectively. The expression of Hsp70 and HSF-1 in liver and renal of YC-1+HS group was significantly higher than that of HS group. All of the protective effects of YC-1 were all significantly suppressed when pretreated with quercetin (400mg/kg). Results indicate that YC-1 may improve survival due to induce Hsp70 overexpression.</description><subject>Animals</subject><subject>Arterial Pressure - drug effects</subject><subject>biomarkers</subject><subject>body temperature</subject><subject>Disease Models, Animal</subject><subject>DNA-Binding Proteins - genetics</subject><subject>Enzyme Activators - pharmacology</subject><subject>Gene Expression Regulation - drug effects</subject><subject>guanylate cyclase</subject><subject>heart rate</subject><subject>Heart Rate - drug effects</subject><subject>Heat shock factor-1</subject><subject>Heat shock protein</subject><subject>Heat shock response</subject><subject>Heat Shock Transcription Factors</subject><subject>heat stress</subject><subject>Heat stroke</subject><subject>Heat Stroke - drug therapy</subject><subject>Heat Stroke - physiopathology</subject><subject>heat-shock protein 70</subject><subject>HSP70 Heat-Shock Proteins - metabolism</subject><subject>Indazoles - pharmacology</subject><subject>Kidney - drug effects</subject><subject>Kidney - pathology</subject><subject>kidneys</subject><subject>liver</subject><subject>Liver - drug effects</subject><subject>Liver - pathology</subject><subject>Male</subject><subject>pharmacology</subject><subject>protective effect</subject><subject>quercetin</subject><subject>Quercetin - pharmacology</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Survival Rate</subject><subject>Transcription Factors - genetics</subject><subject>YC-1</subject><issn>0014-2999</issn><issn>1879-0712</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kMFuEzEQhi0EoqHwBgh85LLLjNdery9IKCoUqRIHWiROluMdE6dJHOxNJd4eh005crGt0ff_Hn2MvUZoEbB_v2lpc1i73ApA0SK2IOUTtsBBmwY0iqdsAYCyEcaYC_ailA0AKCPUc3YhOoFGG71g32_XxHPaEk-Br8lNvKyTv-eHnCaKe66B13Oq0N-Jn-IDcQqhvk6JH8sGedqfk1NO97XNTeUlexbcttCr833J7j5d3S6vm5uvn78sP940XioxNejGvg-m9-B7qSQiDSP0phvACKlW1K_8yoSBdC-dHxFIqa5DlN0YdB0M3SV7N_fW7X4dqUx2F4un7dbtKR2LRTHobtBDJysqZ9TnVEqmYA857lz-bRHsyajd2NmoPRm1iLYarbE35x-Oqx2N_0KPCivwdgaCS9b9zLHYu2-1QVXdEoWCSnyYCaomHiJlW3ykvacx5urRjin-f4c_LXOQQQ</recordid><startdate>20130115</startdate><enddate>20130115</enddate><creator>Lam, Kwok-Keung</creator><creator>Cheng, Pao-Yun</creator><creator>Lee, Yen-Mei</creator><creator>Liu, Yu-Pei</creator><creator>Ding, Cheng</creator><creator>Liu, Won-Hsiung</creator><creator>Yen, Mao-Hsiung</creator><general>Elsevier B.V</general><scope>FBQ</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>7X8</scope></search><sort><creationdate>20130115</creationdate><title>The role of heat shock protein 70 in the protective effect of YC-1 on heat stroke rats</title><author>Lam, Kwok-Keung ; Cheng, Pao-Yun ; Lee, Yen-Mei ; Liu, Yu-Pei ; Ding, Cheng ; Liu, Won-Hsiung ; Yen, Mao-Hsiung</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c452t-1ad66f96c0c645411e8d0693809245be6bcb9f8e764acd10e55331143df7acd83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Animals</topic><topic>Arterial Pressure - drug effects</topic><topic>biomarkers</topic><topic>body temperature</topic><topic>Disease Models, Animal</topic><topic>DNA-Binding Proteins - genetics</topic><topic>Enzyme Activators - pharmacology</topic><topic>Gene Expression Regulation - drug effects</topic><topic>guanylate cyclase</topic><topic>heart rate</topic><topic>Heart Rate - drug effects</topic><topic>Heat shock factor-1</topic><topic>Heat shock protein</topic><topic>Heat shock response</topic><topic>Heat Shock Transcription Factors</topic><topic>heat stress</topic><topic>Heat stroke</topic><topic>Heat Stroke - drug therapy</topic><topic>Heat Stroke - physiopathology</topic><topic>heat-shock protein 70</topic><topic>HSP70 Heat-Shock Proteins - metabolism</topic><topic>Indazoles - pharmacology</topic><topic>Kidney - drug effects</topic><topic>Kidney - pathology</topic><topic>kidneys</topic><topic>liver</topic><topic>Liver - drug effects</topic><topic>Liver - pathology</topic><topic>Male</topic><topic>pharmacology</topic><topic>protective effect</topic><topic>quercetin</topic><topic>Quercetin - pharmacology</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Survival Rate</topic><topic>Transcription Factors - genetics</topic><topic>YC-1</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lam, Kwok-Keung</creatorcontrib><creatorcontrib>Cheng, Pao-Yun</creatorcontrib><creatorcontrib>Lee, Yen-Mei</creatorcontrib><creatorcontrib>Liu, Yu-Pei</creatorcontrib><creatorcontrib>Ding, Cheng</creatorcontrib><creatorcontrib>Liu, Won-Hsiung</creatorcontrib><creatorcontrib>Yen, Mao-Hsiung</creatorcontrib><collection>AGRIS</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>European journal of pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lam, Kwok-Keung</au><au>Cheng, Pao-Yun</au><au>Lee, Yen-Mei</au><au>Liu, Yu-Pei</au><au>Ding, Cheng</au><au>Liu, Won-Hsiung</au><au>Yen, Mao-Hsiung</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The role of heat shock protein 70 in the protective effect of YC-1 on heat stroke rats</atitle><jtitle>European journal of pharmacology</jtitle><addtitle>Eur J Pharmacol</addtitle><date>2013-01-15</date><risdate>2013</risdate><volume>699</volume><issue>1-3</issue><spage>67</spage><epage>73</epage><pages>67-73</pages><issn>0014-2999</issn><eissn>1879-0712</eissn><abstract>Heat stroke is a life-threatening illness characterized by an elevated core body temperature. Despite adequate lowering of the body temperature and support treatment of multiple organ-system function, heat stroke is often fatal. 3-(5′-Hydoxymethyl-2′-furyl)-1-benzyl-indazol (YC-1) been identified as an activator of soluble guanylate cyclase. To evaluate whether YC-1 protects multiple organ dysfunctions and improves survival during heat stroke and its mechanism. Male Sprague-Dawley rats untreated or treated with either YC-1 or quercetin (heat shock protein (Hsp) 70 inhibitor) were exposures to heat as a model of heat stroke. The mean arterial pressure (MAP), heart rate, rectal temperature (Tco), survival time, and plasma biochemical data, intracellular Hsp70 and heat shock factor-1 expression were measured. The value of MAP, heart rate and Tco of untreated heat stroke (HS) group were all significantly lower than that of normothermal (NT) group. Biochemical markers evidenced that liver and kidney injuries of HS group were significantly higher than that of NT groups. YC-1 (20mg/kg) pretreatment with heat stroke (YC-1+HS) group, the MAP and heart rate were return to normal, and the biochemical markers were all significantly recovered to normal. The survival time of HS group, NT group and YC-1+HS group were 21, 480, and 445min, respectively. The expression of Hsp70 and HSF-1 in liver and renal of YC-1+HS group was significantly higher than that of HS group. All of the protective effects of YC-1 were all significantly suppressed when pretreated with quercetin (400mg/kg). Results indicate that YC-1 may improve survival due to induce Hsp70 overexpression.</abstract><cop>Netherlands</cop><pub>Elsevier B.V</pub><pmid>23219797</pmid><doi>10.1016/j.ejphar.2012.11.044</doi><tpages>7</tpages></addata></record> |
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| subjects | Animals Arterial Pressure - drug effects biomarkers body temperature Disease Models, Animal DNA-Binding Proteins - genetics Enzyme Activators - pharmacology Gene Expression Regulation - drug effects guanylate cyclase heart rate Heart Rate - drug effects Heat shock factor-1 Heat shock protein Heat shock response Heat Shock Transcription Factors heat stress Heat stroke Heat Stroke - drug therapy Heat Stroke - physiopathology heat-shock protein 70 HSP70 Heat-Shock Proteins - metabolism Indazoles - pharmacology Kidney - drug effects Kidney - pathology kidneys liver Liver - drug effects Liver - pathology Male pharmacology protective effect quercetin Quercetin - pharmacology Rats Rats, Sprague-Dawley Survival Rate Transcription Factors - genetics YC-1 |
| title | The role of heat shock protein 70 in the protective effect of YC-1 on heat stroke rats |
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