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trans-Polydatin protects the mouse heart against ischemia/reperfusion injury via inhibition of the renin-angiotensin system (RAS) and Rho kinase (ROCK) activity
Recent studies highlighted the protective benefits of a Chinese herb extract from polygonum cuspidatum, trans-polydatin, on cardiac disease. We investigated the therapeutic effect of trans-polydatin on myocardial ischemia/reperfusion (IR) injury and the underlying mechanisms related to the renin-ang...
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Published in: | Food & function 2017-06, Vol.8 (6), p.2309-2321 |
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creator | Ming, Dong Songyan, Liao Yawen, Chen Na, Zheng Jing, Ma Zhaowen, Xiao Ye, Liu Wa, Ding Jie, Liu |
description | Recent studies highlighted the protective benefits of a Chinese herb extract from polygonum cuspidatum, trans-polydatin, on cardiac disease. We investigated the therapeutic effect of trans-polydatin on myocardial ischemia/reperfusion (IR) injury and the underlying mechanisms related to the renin-angiotensin system (RAS) and RhoA kinase (ROCK) pathway.
Experiments were performed on neonatal rats' ventricular myocytes that were subjected to hypoxia-reoxygenation (simulated IR, SIR) and on adult mice which were subjected to left anterior descending coronary artery occlusion for 45 min followed by a one-week reperfusion. trans-Polydatin significantly increased cell viability and reduced apoptosis in SIR cardiomyocytes. It was also observed to reduce the infarct size and increase the cardiac function in IR mice. trans-Polydatin decreased the expression of angiotensin and inhibited the activities of renin and angiotensin-converting enzyme. Furthermore, trans-polydatin inhibited ROCK activity, especially the angiotensin I receptor-activated ROCK pathway.
trans-Polydatin exerts a cardio-protection against myocardial IR injury likely through inhibiting both RAS and the downstream ROCK pathway. |
doi_str_mv | 10.1039/c6fo01842d |
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Experiments were performed on neonatal rats' ventricular myocytes that were subjected to hypoxia-reoxygenation (simulated IR, SIR) and on adult mice which were subjected to left anterior descending coronary artery occlusion for 45 min followed by a one-week reperfusion. trans-Polydatin significantly increased cell viability and reduced apoptosis in SIR cardiomyocytes. It was also observed to reduce the infarct size and increase the cardiac function in IR mice. trans-Polydatin decreased the expression of angiotensin and inhibited the activities of renin and angiotensin-converting enzyme. Furthermore, trans-polydatin inhibited ROCK activity, especially the angiotensin I receptor-activated ROCK pathway.
trans-Polydatin exerts a cardio-protection against myocardial IR injury likely through inhibiting both RAS and the downstream ROCK pathway.</description><identifier>ISSN: 2042-6496</identifier><identifier>EISSN: 2042-650X</identifier><identifier>DOI: 10.1039/c6fo01842d</identifier><identifier>PMID: 28589995</identifier><language>eng</language><publisher>England</publisher><subject>Animals ; Apoptosis - drug effects ; Glucosides - administration & dosage ; Glucosides - chemistry ; Heart - drug effects ; Humans ; Ischemia - surgery ; Male ; Mice ; Mice, Inbred C57BL ; Myocardial Reperfusion Injury - drug therapy ; Myocardial Reperfusion Injury - enzymology ; Myocardial Reperfusion Injury - genetics ; Myocardial Reperfusion Injury - metabolism ; Myocardium - metabolism ; Polygonum cuspidatum ; Renin-Angiotensin System - drug effects ; rho-Associated Kinases - metabolism ; Signal Transduction - drug effects ; Stilbenes - administration & dosage ; Stilbenes - chemistry</subject><ispartof>Food & function, 2017-06, Vol.8 (6), p.2309-2321</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c320t-23b602c834584356980a22b6e0359ade67d7679c2cd3839f69715af52c214d843</citedby><cites>FETCH-LOGICAL-c320t-23b602c834584356980a22b6e0359ade67d7679c2cd3839f69715af52c214d843</cites><orcidid>0000-0002-6608-840X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28589995$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ming, Dong</creatorcontrib><creatorcontrib>Songyan, Liao</creatorcontrib><creatorcontrib>Yawen, Chen</creatorcontrib><creatorcontrib>Na, Zheng</creatorcontrib><creatorcontrib>Jing, Ma</creatorcontrib><creatorcontrib>Zhaowen, Xiao</creatorcontrib><creatorcontrib>Ye, Liu</creatorcontrib><creatorcontrib>Wa, Ding</creatorcontrib><creatorcontrib>Jie, Liu</creatorcontrib><title>trans-Polydatin protects the mouse heart against ischemia/reperfusion injury via inhibition of the renin-angiotensin system (RAS) and Rho kinase (ROCK) activity</title><title>Food & function</title><addtitle>Food Funct</addtitle><description>Recent studies highlighted the protective benefits of a Chinese herb extract from polygonum cuspidatum, trans-polydatin, on cardiac disease. We investigated the therapeutic effect of trans-polydatin on myocardial ischemia/reperfusion (IR) injury and the underlying mechanisms related to the renin-angiotensin system (RAS) and RhoA kinase (ROCK) pathway.
Experiments were performed on neonatal rats' ventricular myocytes that were subjected to hypoxia-reoxygenation (simulated IR, SIR) and on adult mice which were subjected to left anterior descending coronary artery occlusion for 45 min followed by a one-week reperfusion. trans-Polydatin significantly increased cell viability and reduced apoptosis in SIR cardiomyocytes. It was also observed to reduce the infarct size and increase the cardiac function in IR mice. trans-Polydatin decreased the expression of angiotensin and inhibited the activities of renin and angiotensin-converting enzyme. Furthermore, trans-polydatin inhibited ROCK activity, especially the angiotensin I receptor-activated ROCK pathway.
trans-Polydatin exerts a cardio-protection against myocardial IR injury likely through inhibiting both RAS and the downstream ROCK pathway.</description><subject>Animals</subject><subject>Apoptosis - drug effects</subject><subject>Glucosides - administration & dosage</subject><subject>Glucosides - chemistry</subject><subject>Heart - drug effects</subject><subject>Humans</subject><subject>Ischemia - surgery</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Myocardial Reperfusion Injury - drug therapy</subject><subject>Myocardial Reperfusion Injury - enzymology</subject><subject>Myocardial Reperfusion Injury - genetics</subject><subject>Myocardial Reperfusion Injury - metabolism</subject><subject>Myocardium - metabolism</subject><subject>Polygonum cuspidatum</subject><subject>Renin-Angiotensin System - drug effects</subject><subject>rho-Associated Kinases - metabolism</subject><subject>Signal Transduction - drug effects</subject><subject>Stilbenes - administration & dosage</subject><subject>Stilbenes - chemistry</subject><issn>2042-6496</issn><issn>2042-650X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><recordid>eNqNkc9u2zAMxoVhwxp0uewBBh2zAm5lyZKlY5Ctf9ACKdIN2M1QZLpWF8upJBfw2_RRqzTJzuOFBPHjR5AfQl9zcp4Tpi6MaHqSy4LWH9CEkoJmgpM_H491ocQJmobwRFIwpaSSn9EJlVwqpfgEvUavXcju-81Y62gd3vo-gokBxxZw1w8BcAvaR6wftXUhYhtMC53VFx624Jsh2N5h654GP-IXq1PZ2rWNu27fvKt4cNZl2j3aJO1CWhLGEKHDs9X84TvWrsartsd_rdNp22y1XNymron2xcbxC_rU6E2A6SGfot-XP38trrO75dXNYn6XGUZJzChbC0KNZAWXBeNCSaIpXQsgjCtdgyjrUpTKUFMzyVQjVJlz3XBqaF7UaeQUzfa66QHPA4RYdelS2Gy0g_SFKle5YKVUQvwHSkpCKC926NkeNb4PwUNTbb3ttB-rnFQ7_6qFuFy--_cjwd8OusO6g_ofenSLvQGc1JZq</recordid><startdate>20170601</startdate><enddate>20170601</enddate><creator>Ming, Dong</creator><creator>Songyan, Liao</creator><creator>Yawen, Chen</creator><creator>Na, Zheng</creator><creator>Jing, Ma</creator><creator>Zhaowen, Xiao</creator><creator>Ye, Liu</creator><creator>Wa, Ding</creator><creator>Jie, Liu</creator><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>7T5</scope><scope>7TO</scope><scope>H94</scope><orcidid>https://orcid.org/0000-0002-6608-840X</orcidid></search><sort><creationdate>20170601</creationdate><title>trans-Polydatin protects the mouse heart against ischemia/reperfusion injury via inhibition of the renin-angiotensin system (RAS) and Rho kinase (ROCK) activity</title><author>Ming, Dong ; Songyan, Liao ; Yawen, Chen ; Na, Zheng ; Jing, Ma ; Zhaowen, Xiao ; Ye, Liu ; Wa, Ding ; Jie, Liu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c320t-23b602c834584356980a22b6e0359ade67d7679c2cd3839f69715af52c214d843</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Animals</topic><topic>Apoptosis - drug effects</topic><topic>Glucosides - administration & dosage</topic><topic>Glucosides - chemistry</topic><topic>Heart - drug effects</topic><topic>Humans</topic><topic>Ischemia - surgery</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Myocardial Reperfusion Injury - drug therapy</topic><topic>Myocardial Reperfusion Injury - enzymology</topic><topic>Myocardial Reperfusion Injury - genetics</topic><topic>Myocardial Reperfusion Injury - metabolism</topic><topic>Myocardium - metabolism</topic><topic>Polygonum cuspidatum</topic><topic>Renin-Angiotensin System - drug effects</topic><topic>rho-Associated Kinases - metabolism</topic><topic>Signal Transduction - drug effects</topic><topic>Stilbenes - administration & dosage</topic><topic>Stilbenes - chemistry</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ming, Dong</creatorcontrib><creatorcontrib>Songyan, Liao</creatorcontrib><creatorcontrib>Yawen, Chen</creatorcontrib><creatorcontrib>Na, Zheng</creatorcontrib><creatorcontrib>Jing, Ma</creatorcontrib><creatorcontrib>Zhaowen, Xiao</creatorcontrib><creatorcontrib>Ye, Liu</creatorcontrib><creatorcontrib>Wa, Ding</creatorcontrib><creatorcontrib>Jie, Liu</creatorcontrib><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>Immunology Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><jtitle>Food & function</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ming, Dong</au><au>Songyan, Liao</au><au>Yawen, Chen</au><au>Na, Zheng</au><au>Jing, Ma</au><au>Zhaowen, Xiao</au><au>Ye, Liu</au><au>Wa, Ding</au><au>Jie, Liu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>trans-Polydatin protects the mouse heart against ischemia/reperfusion injury via inhibition of the renin-angiotensin system (RAS) and Rho kinase (ROCK) activity</atitle><jtitle>Food & function</jtitle><addtitle>Food Funct</addtitle><date>2017-06-01</date><risdate>2017</risdate><volume>8</volume><issue>6</issue><spage>2309</spage><epage>2321</epage><pages>2309-2321</pages><issn>2042-6496</issn><eissn>2042-650X</eissn><abstract>Recent studies highlighted the protective benefits of a Chinese herb extract from polygonum cuspidatum, trans-polydatin, on cardiac disease. We investigated the therapeutic effect of trans-polydatin on myocardial ischemia/reperfusion (IR) injury and the underlying mechanisms related to the renin-angiotensin system (RAS) and RhoA kinase (ROCK) pathway.
Experiments were performed on neonatal rats' ventricular myocytes that were subjected to hypoxia-reoxygenation (simulated IR, SIR) and on adult mice which were subjected to left anterior descending coronary artery occlusion for 45 min followed by a one-week reperfusion. trans-Polydatin significantly increased cell viability and reduced apoptosis in SIR cardiomyocytes. It was also observed to reduce the infarct size and increase the cardiac function in IR mice. trans-Polydatin decreased the expression of angiotensin and inhibited the activities of renin and angiotensin-converting enzyme. Furthermore, trans-polydatin inhibited ROCK activity, especially the angiotensin I receptor-activated ROCK pathway.
trans-Polydatin exerts a cardio-protection against myocardial IR injury likely through inhibiting both RAS and the downstream ROCK pathway.</abstract><cop>England</cop><pmid>28589995</pmid><doi>10.1039/c6fo01842d</doi><tpages>13</tpages><orcidid>https://orcid.org/0000-0002-6608-840X</orcidid></addata></record> |
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subjects | Animals Apoptosis - drug effects Glucosides - administration & dosage Glucosides - chemistry Heart - drug effects Humans Ischemia - surgery Male Mice Mice, Inbred C57BL Myocardial Reperfusion Injury - drug therapy Myocardial Reperfusion Injury - enzymology Myocardial Reperfusion Injury - genetics Myocardial Reperfusion Injury - metabolism Myocardium - metabolism Polygonum cuspidatum Renin-Angiotensin System - drug effects rho-Associated Kinases - metabolism Signal Transduction - drug effects Stilbenes - administration & dosage Stilbenes - chemistry |
title | trans-Polydatin protects the mouse heart against ischemia/reperfusion injury via inhibition of the renin-angiotensin system (RAS) and Rho kinase (ROCK) activity |
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