The Protective Effects of Salidroside from Exhaustive Exercise-Induced Heart Injury by Enhancing the PGC-1α–NRF1/NRF2 Pathway and Mitochondrial Respiratory Function in Rats
Objective. To test the hypothesis that salidroside (SAL) can protect heart from exhaustive exercise-induced injury by enhancing mitochondrial respiratory function and mitochondrial biogenesis key signaling pathway PGC-1α–NRF1/NRF2 in rats. Methods. Male Sprague-Dawley rats were divided into 4 groups...
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| creator | Cao, Xuebin Wang, Dong-ying Xu, Peng Meng, Zhen-zhi Jiang, Cai-wu Chang, Yu-mei Cui, Yu-juan Zhang, Long-fei Ping, Zheng Liu, Hai-yan |
| description | Objective. To test the hypothesis that salidroside (SAL) can protect heart from exhaustive exercise-induced injury by enhancing mitochondrial respiratory function and mitochondrial biogenesis key signaling pathway PGC-1α–NRF1/NRF2 in rats. Methods. Male Sprague-Dawley rats were divided into 4 groups: sedentary (C), exhaustive exercise (EE), low-dose SAL (LS), and high-dose SAL (HS). After one-time exhaustive swimming exercise, we measured the changes in cardiomyocyte ultrastructure and cardiac marker enzymes and mitochondrial electron transport system (ETS) complexes activities in situ. We also measured mitochondrial biogenesis master regulator PGC-1α and its downstream transcription factors, NRF1 and NRF2, expression at gene and protein levels. Results. Compared to C group, the EE group showed marked myocardium ultrastructure injury and decrease of mitochondrial respiratory function P |
| doi_str_mv | 10.1155/2015/876825 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_4488012</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A454270461</galeid><sourcerecordid>A454270461</sourcerecordid><originalsourceid>FETCH-LOGICAL-c360t-1e69f72bf55eb2e9b455e1546542819103462dfcfe5401148bf1f245eda5e4da3</originalsourceid><addsrcrecordid>eNqNksFqFDEcxgdRbK2evEvAiyjjJplkduYilGW3Xaha1noOmeSfTspssk1m2u7Nd_BBxBfxIXwSs0xd6s1L8kF-fPng-7LsJcHvCeF8QjHhk2paVpQ_yg5JzWiO65o93muMD7JnMV5hXBaUkafZAS1JOaWMHmY_LlpA58H3oHp7A2huTFIReYO-yM7q4KPVgEzwazS_a-UQR-wOgrIR8qXTgwKNTkGGHi3d1RC2qNmiuWulU9Zdon73wcksJ79-_v72_dNqQSbpoOhc9u2t3CLpNPpoe69a73SwskMriBsbZO-T1WJwKZh3yDq0kn18nj0xsovw4v4-yr4u5hez0_zs88lydnyWq6LEfU6grM2UNoZzaCjUDUuCcFZyRitSE1ywkmqjDHCGCWFVY4ihjIOWHJiWxVH2YfTdDM0atALXB9mJTbBrGbbCSyv-fXG2FZf-RjBWVZjQZPDm3iD46wFiL9Y2Kug66cAPUZCyLlM_jOKEvh7RS9mBsM745Kh2uDhmKfAUs5Ik6t1IqdRJDGD2YQgWuyGI3RDEOIREv3qYf8_-bT4Bb0egtU7LW_t_bpAQMPIBPOUVLoo_HbTHeQ</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1696194420</pqid></control><display><type>article</type><title>The Protective Effects of Salidroside from Exhaustive Exercise-Induced Heart Injury by Enhancing the PGC-1α–NRF1/NRF2 Pathway and Mitochondrial Respiratory Function in Rats</title><source>MEDLINE</source><source>Wiley Online Library Open Access</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>PubMed Central</source><source>Alma/SFX Local Collection</source><source>PubMed Central Open Access</source><creator>Cao, Xuebin ; Wang, Dong-ying ; Xu, Peng ; Meng, Zhen-zhi ; Jiang, Cai-wu ; Chang, Yu-mei ; Cui, Yu-juan ; Zhang, Long-fei ; Ping, Zheng ; Liu, Hai-yan</creator><contributor>Chen, Yanfang</contributor><creatorcontrib>Cao, Xuebin ; Wang, Dong-ying ; Xu, Peng ; Meng, Zhen-zhi ; Jiang, Cai-wu ; Chang, Yu-mei ; Cui, Yu-juan ; Zhang, Long-fei ; Ping, Zheng ; Liu, Hai-yan ; Chen, Yanfang</creatorcontrib><description>Objective. To test the hypothesis that salidroside (SAL) can protect heart from exhaustive exercise-induced injury by enhancing mitochondrial respiratory function and mitochondrial biogenesis key signaling pathway PGC-1α–NRF1/NRF2 in rats. Methods. Male Sprague-Dawley rats were divided into 4 groups: sedentary (C), exhaustive exercise (EE), low-dose SAL (LS), and high-dose SAL (HS). After one-time exhaustive swimming exercise, we measured the changes in cardiomyocyte ultrastructure and cardiac marker enzymes and mitochondrial electron transport system (ETS) complexes activities in situ. We also measured mitochondrial biogenesis master regulator PGC-1α and its downstream transcription factors, NRF1 and NRF2, expression at gene and protein levels. Results. Compared to C group, the EE group showed marked myocardium ultrastructure injury and decrease of mitochondrial respiratory function P<0.05 and protein levels of PGC-1α, NRF1, and NRF2 P<0.05 but a significant increase of PGC-1α, NRF1, and NRF2 genes levels P<0.05; compared to EE group, SAL ameliorated myocardium injury, increased mitochondrial respiratory function P<0.05, and elevated both gene and protein levels of PGC-1α, NRF-1, and NRF-2. Conclusion. Salidroside can protect the heart from exhaustive exercise-induced injury. It might act by improving myocardial mitochondrial respiratory function by stimulating the expression of PGC-1α–NRF1/NRF2 pathway.</description><identifier>ISSN: 1942-0900</identifier><identifier>EISSN: 1942-0994</identifier><identifier>DOI: 10.1155/2015/876825</identifier><identifier>PMID: 26167242</identifier><language>eng</language><publisher>Cairo, Egypt: Hindawi Publishing Corporation</publisher><subject>Animals ; Biosynthesis ; Electron transport ; Electron Transport Chain Complex Proteins - metabolism ; Enzymes ; Gene Expression Regulation - drug effects ; Genes ; Genetic transcription ; Glucosides - pharmacology ; Glucosides - therapeutic use ; Heart Injuries - drug therapy ; Heart Injuries - etiology ; Male ; Mitochondria - drug effects ; Mitochondria - metabolism ; Muscle, Skeletal - ultrastructure ; Myocardium - metabolism ; Myocardium - pathology ; NF-E2-Related Factor 2 - genetics ; NF-E2-Related Factor 2 - metabolism ; Nuclear Respiratory Factor 1 - genetics ; Nuclear Respiratory Factor 1 - metabolism ; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha ; Phenols - pharmacology ; Phenols - therapeutic use ; Physical Conditioning, Animal ; Rats ; Rats, Sprague-Dawley ; Signal Transduction - drug effects ; Transcription Factors - genetics ; Transcription Factors - metabolism</subject><ispartof>Oxidative medicine and cellular longevity, 2015-01, Vol.2015 (2015), p.1-9</ispartof><rights>Copyright © 2015 Zheng Ping et al.</rights><rights>COPYRIGHT 2015 John Wiley & Sons, Inc.</rights><rights>Copyright © 2015 Zheng Ping et al. 2015</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c360t-1e69f72bf55eb2e9b455e1546542819103462dfcfe5401148bf1f245eda5e4da3</citedby><cites>FETCH-LOGICAL-c360t-1e69f72bf55eb2e9b455e1546542819103462dfcfe5401148bf1f245eda5e4da3</cites><orcidid>0000-0002-9056-1826</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4488012/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4488012/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26167242$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Chen, Yanfang</contributor><creatorcontrib>Cao, Xuebin</creatorcontrib><creatorcontrib>Wang, Dong-ying</creatorcontrib><creatorcontrib>Xu, Peng</creatorcontrib><creatorcontrib>Meng, Zhen-zhi</creatorcontrib><creatorcontrib>Jiang, Cai-wu</creatorcontrib><creatorcontrib>Chang, Yu-mei</creatorcontrib><creatorcontrib>Cui, Yu-juan</creatorcontrib><creatorcontrib>Zhang, Long-fei</creatorcontrib><creatorcontrib>Ping, Zheng</creatorcontrib><creatorcontrib>Liu, Hai-yan</creatorcontrib><title>The Protective Effects of Salidroside from Exhaustive Exercise-Induced Heart Injury by Enhancing the PGC-1α–NRF1/NRF2 Pathway and Mitochondrial Respiratory Function in Rats</title><title>Oxidative medicine and cellular longevity</title><addtitle>Oxid Med Cell Longev</addtitle><description>Objective. To test the hypothesis that salidroside (SAL) can protect heart from exhaustive exercise-induced injury by enhancing mitochondrial respiratory function and mitochondrial biogenesis key signaling pathway PGC-1α–NRF1/NRF2 in rats. Methods. Male Sprague-Dawley rats were divided into 4 groups: sedentary (C), exhaustive exercise (EE), low-dose SAL (LS), and high-dose SAL (HS). After one-time exhaustive swimming exercise, we measured the changes in cardiomyocyte ultrastructure and cardiac marker enzymes and mitochondrial electron transport system (ETS) complexes activities in situ. We also measured mitochondrial biogenesis master regulator PGC-1α and its downstream transcription factors, NRF1 and NRF2, expression at gene and protein levels. Results. Compared to C group, the EE group showed marked myocardium ultrastructure injury and decrease of mitochondrial respiratory function P<0.05 and protein levels of PGC-1α, NRF1, and NRF2 P<0.05 but a significant increase of PGC-1α, NRF1, and NRF2 genes levels P<0.05; compared to EE group, SAL ameliorated myocardium injury, increased mitochondrial respiratory function P<0.05, and elevated both gene and protein levels of PGC-1α, NRF-1, and NRF-2. Conclusion. Salidroside can protect the heart from exhaustive exercise-induced injury. It might act by improving myocardial mitochondrial respiratory function by stimulating the expression of PGC-1α–NRF1/NRF2 pathway.</description><subject>Animals</subject><subject>Biosynthesis</subject><subject>Electron transport</subject><subject>Electron Transport Chain Complex Proteins - metabolism</subject><subject>Enzymes</subject><subject>Gene Expression Regulation - drug effects</subject><subject>Genes</subject><subject>Genetic transcription</subject><subject>Glucosides - pharmacology</subject><subject>Glucosides - therapeutic use</subject><subject>Heart Injuries - drug therapy</subject><subject>Heart Injuries - etiology</subject><subject>Male</subject><subject>Mitochondria - drug effects</subject><subject>Mitochondria - metabolism</subject><subject>Muscle, Skeletal - ultrastructure</subject><subject>Myocardium - metabolism</subject><subject>Myocardium - pathology</subject><subject>NF-E2-Related Factor 2 - genetics</subject><subject>NF-E2-Related Factor 2 - metabolism</subject><subject>Nuclear Respiratory Factor 1 - genetics</subject><subject>Nuclear Respiratory Factor 1 - metabolism</subject><subject>Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha</subject><subject>Phenols - pharmacology</subject><subject>Phenols - therapeutic use</subject><subject>Physical Conditioning, Animal</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Signal Transduction - drug effects</subject><subject>Transcription Factors - genetics</subject><subject>Transcription Factors - metabolism</subject><issn>1942-0900</issn><issn>1942-0994</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>RHX</sourceid><sourceid>EIF</sourceid><recordid>eNqNksFqFDEcxgdRbK2evEvAiyjjJplkduYilGW3Xaha1noOmeSfTspssk1m2u7Nd_BBxBfxIXwSs0xd6s1L8kF-fPng-7LsJcHvCeF8QjHhk2paVpQ_yg5JzWiO65o93muMD7JnMV5hXBaUkafZAS1JOaWMHmY_LlpA58H3oHp7A2huTFIReYO-yM7q4KPVgEzwazS_a-UQR-wOgrIR8qXTgwKNTkGGHi3d1RC2qNmiuWulU9Zdon73wcksJ79-_v72_dNqQSbpoOhc9u2t3CLpNPpoe69a73SwskMriBsbZO-T1WJwKZh3yDq0kn18nj0xsovw4v4-yr4u5hez0_zs88lydnyWq6LEfU6grM2UNoZzaCjUDUuCcFZyRitSE1ywkmqjDHCGCWFVY4ihjIOWHJiWxVH2YfTdDM0atALXB9mJTbBrGbbCSyv-fXG2FZf-RjBWVZjQZPDm3iD46wFiL9Y2Kug66cAPUZCyLlM_jOKEvh7RS9mBsM745Kh2uDhmKfAUs5Ik6t1IqdRJDGD2YQgWuyGI3RDEOIREv3qYf8_-bT4Bb0egtU7LW_t_bpAQMPIBPOUVLoo_HbTHeQ</recordid><startdate>20150101</startdate><enddate>20150101</enddate><creator>Cao, Xuebin</creator><creator>Wang, Dong-ying</creator><creator>Xu, Peng</creator><creator>Meng, Zhen-zhi</creator><creator>Jiang, Cai-wu</creator><creator>Chang, Yu-mei</creator><creator>Cui, Yu-juan</creator><creator>Zhang, Long-fei</creator><creator>Ping, Zheng</creator><creator>Liu, Hai-yan</creator><general>Hindawi Publishing Corporation</general><general>John Wiley & Sons, Inc</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>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-9056-1826</orcidid></search><sort><creationdate>20150101</creationdate><title>The Protective Effects of Salidroside from Exhaustive Exercise-Induced Heart Injury by Enhancing the PGC-1α–NRF1/NRF2 Pathway and Mitochondrial Respiratory Function in Rats</title><author>Cao, Xuebin ; Wang, Dong-ying ; Xu, Peng ; Meng, Zhen-zhi ; Jiang, Cai-wu ; Chang, Yu-mei ; Cui, Yu-juan ; Zhang, Long-fei ; Ping, Zheng ; Liu, Hai-yan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c360t-1e69f72bf55eb2e9b455e1546542819103462dfcfe5401148bf1f245eda5e4da3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Animals</topic><topic>Biosynthesis</topic><topic>Electron transport</topic><topic>Electron Transport Chain Complex Proteins - metabolism</topic><topic>Enzymes</topic><topic>Gene Expression Regulation - drug effects</topic><topic>Genes</topic><topic>Genetic transcription</topic><topic>Glucosides - pharmacology</topic><topic>Glucosides - therapeutic use</topic><topic>Heart Injuries - drug therapy</topic><topic>Heart Injuries - etiology</topic><topic>Male</topic><topic>Mitochondria - drug effects</topic><topic>Mitochondria - metabolism</topic><topic>Muscle, Skeletal - ultrastructure</topic><topic>Myocardium - metabolism</topic><topic>Myocardium - pathology</topic><topic>NF-E2-Related Factor 2 - genetics</topic><topic>NF-E2-Related Factor 2 - metabolism</topic><topic>Nuclear Respiratory Factor 1 - genetics</topic><topic>Nuclear Respiratory Factor 1 - metabolism</topic><topic>Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha</topic><topic>Phenols - pharmacology</topic><topic>Phenols - therapeutic use</topic><topic>Physical Conditioning, Animal</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Signal Transduction - drug effects</topic><topic>Transcription Factors - genetics</topic><topic>Transcription Factors - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Cao, Xuebin</creatorcontrib><creatorcontrib>Wang, Dong-ying</creatorcontrib><creatorcontrib>Xu, Peng</creatorcontrib><creatorcontrib>Meng, Zhen-zhi</creatorcontrib><creatorcontrib>Jiang, Cai-wu</creatorcontrib><creatorcontrib>Chang, Yu-mei</creatorcontrib><creatorcontrib>Cui, Yu-juan</creatorcontrib><creatorcontrib>Zhang, Long-fei</creatorcontrib><creatorcontrib>Ping, Zheng</creatorcontrib><creatorcontrib>Liu, Hai-yan</creatorcontrib><collection>الدوريات العلمية والإحصائية - e-Marefa Academic and Statistical Periodicals</collection><collection>معرفة - المحتوى العربي الأكاديمي المتكامل - e-Marefa Academic Complete</collection><collection>Hindawi Publishing Complete</collection><collection>Hindawi Publishing Subscription Journals</collection><collection>Hindawi Publishing Open Access</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><collection>PubMed Central (Full Participant titles)</collection><jtitle>Oxidative medicine and cellular longevity</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Cao, Xuebin</au><au>Wang, Dong-ying</au><au>Xu, Peng</au><au>Meng, Zhen-zhi</au><au>Jiang, Cai-wu</au><au>Chang, Yu-mei</au><au>Cui, Yu-juan</au><au>Zhang, Long-fei</au><au>Ping, Zheng</au><au>Liu, Hai-yan</au><au>Chen, Yanfang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The Protective Effects of Salidroside from Exhaustive Exercise-Induced Heart Injury by Enhancing the PGC-1α–NRF1/NRF2 Pathway and Mitochondrial Respiratory Function in Rats</atitle><jtitle>Oxidative medicine and cellular longevity</jtitle><addtitle>Oxid Med Cell Longev</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>1942-0900</issn><eissn>1942-0994</eissn><abstract>Objective. To test the hypothesis that salidroside (SAL) can protect heart from exhaustive exercise-induced injury by enhancing mitochondrial respiratory function and mitochondrial biogenesis key signaling pathway PGC-1α–NRF1/NRF2 in rats. Methods. Male Sprague-Dawley rats were divided into 4 groups: sedentary (C), exhaustive exercise (EE), low-dose SAL (LS), and high-dose SAL (HS). After one-time exhaustive swimming exercise, we measured the changes in cardiomyocyte ultrastructure and cardiac marker enzymes and mitochondrial electron transport system (ETS) complexes activities in situ. We also measured mitochondrial biogenesis master regulator PGC-1α and its downstream transcription factors, NRF1 and NRF2, expression at gene and protein levels. Results. Compared to C group, the EE group showed marked myocardium ultrastructure injury and decrease of mitochondrial respiratory function P<0.05 and protein levels of PGC-1α, NRF1, and NRF2 P<0.05 but a significant increase of PGC-1α, NRF1, and NRF2 genes levels P<0.05; compared to EE group, SAL ameliorated myocardium injury, increased mitochondrial respiratory function P<0.05, and elevated both gene and protein levels of PGC-1α, NRF-1, and NRF-2. Conclusion. Salidroside can protect the heart from exhaustive exercise-induced injury. It might act by improving myocardial mitochondrial respiratory function by stimulating the expression of PGC-1α–NRF1/NRF2 pathway.</abstract><cop>Cairo, Egypt</cop><pub>Hindawi Publishing Corporation</pub><pmid>26167242</pmid><doi>10.1155/2015/876825</doi><tpages>9</tpages><orcidid>https://orcid.org/0000-0002-9056-1826</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Biosynthesis Electron transport Electron Transport Chain Complex Proteins - metabolism Enzymes Gene Expression Regulation - drug effects Genes Genetic transcription Glucosides - pharmacology Glucosides - therapeutic use Heart Injuries - drug therapy Heart Injuries - etiology Male Mitochondria - drug effects Mitochondria - metabolism Muscle, Skeletal - ultrastructure Myocardium - metabolism Myocardium - pathology NF-E2-Related Factor 2 - genetics NF-E2-Related Factor 2 - metabolism Nuclear Respiratory Factor 1 - genetics Nuclear Respiratory Factor 1 - metabolism Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha Phenols - pharmacology Phenols - therapeutic use Physical Conditioning, Animal Rats Rats, Sprague-Dawley Signal Transduction - drug effects Transcription Factors - genetics Transcription Factors - metabolism |
| title | The Protective Effects of Salidroside from Exhaustive Exercise-Induced Heart Injury by Enhancing the PGC-1α–NRF1/NRF2 Pathway and Mitochondrial Respiratory Function in Rats |
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