Tranilast prevents doxorubicin-induced myocardial hypertrophy and angiotensin II synthesis in rats
An increase in oxidative stress is an important pathological mechanism of heart injury induced by doxorubicin (DOX). Tranilast is an anti-allergy drug that has been shown to possess good antioxidant activity in previous studies. The overexpression and secretion of chymase by mast cells (MCs) increas...
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| Veröffentlicht in: | Life sciences (1973) 2021-02, Vol.267, p.118984, Article 118984 |
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| creator | Zhan, Chengchuang Bai, Nan Zheng, Min Wang, Yanyan Wang, Yuanqi Zhang, Li Li, Jianqiang Li, Guangnan Zhao, Hongyan Liu, Guangzhong Lou, Qi Yang, Wen Li, Tiankai Li, Luyifei Li, Weimin |
| description | An increase in oxidative stress is an important pathological mechanism of heart injury induced by doxorubicin (DOX). Tranilast is an anti-allergy drug that has been shown to possess good antioxidant activity in previous studies. The overexpression and secretion of chymase by mast cells (MCs) increase the pathological overexpression of angiotensin II (Ang II), which plays a crucial role in myocardial hypertrophy and the deterioration of heart disease. The MC stabilizer tranilast (N-(3,4-dimethoxycinnamoyl) anthranilic acid; tran) prevents mast cells from degranulating, which may reduce DOX-induced Ang II synthesis. Therefore, in the present study, we hypothesized that tranilast will protect rats from DOX-induced myocardial damage via its antioxidant activity, thereby inhibiting Ang II expression. Thirty male Wistar rats were divided into three groups (n = 10 in each group) that received DOX, a combination of DOX and tranilast or saline (the control group) to test this hypothesis. Tranilast suppressed chymase expression, reduced Ang II levels and prevented the myocardial hypertrophy and the deterioration of heart function induced by DOX. Based on the findings of the present study, the suppression of chymase-dependent Ang-II production and the direct effect of tranilast on the inhibition of apoptosis and fibrosis because of its antioxidant stress capacity may contribute to the protective effect of tranilast against DOX-induced myocardial hypertrophy.
•Tranilast attenuates the cardiac hypertrophy induced by DOX.•Tranilast prevents the deterioration of heart function induced by DOX.•Tranilast inhibits the expression of Ang II induced by DOX.•Tranilast attenuates oxidative stress and fibrosis induced by DOX. |
| doi_str_mv | 10.1016/j.lfs.2020.118984 |
| format | Article |
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•Tranilast attenuates the cardiac hypertrophy induced by DOX.•Tranilast prevents the deterioration of heart function induced by DOX.•Tranilast inhibits the expression of Ang II induced by DOX.•Tranilast attenuates oxidative stress and fibrosis induced by DOX.</description><identifier>ISSN: 0024-3205</identifier><identifier>EISSN: 1879-0631</identifier><identifier>DOI: 10.1016/j.lfs.2020.118984</identifier><identifier>PMID: 33383049</identifier><language>eng</language><publisher>Netherlands: Elsevier Inc</publisher><subject>Allergies ; Angiotensin ; Angiotensin II ; Angiotensin II - biosynthesis ; Angiotensin II - drug effects ; Angiotensin II - metabolism ; Animals ; Anthranilic acid ; antioxidant activity ; Antioxidants ; Antioxidants - pharmacology ; Apoptosis ; Cardiomegaly - drug therapy ; Cardiomegaly - metabolism ; Cardiovascular diseases ; Chymase ; Coronary artery disease ; Deterioration ; Doxorubicin ; Doxorubicin - adverse effects ; Doxorubicin - pharmacology ; Fibrosis ; heart ; Heart diseases ; Heart Diseases - etiology ; Heart function ; Hypertrophy ; Male ; males ; Mast cells ; Mast Cells - drug effects ; Myocardial hypertrophy ; Myocardium - metabolism ; ortho-Aminobenzoates - metabolism ; ortho-Aminobenzoates - pharmacology ; Oxidative stress ; Oxidative Stress - drug effects ; protective effect ; Rats ; Rats, Wistar ; secretion ; stabilizers ; Synthesis ; Tranilast</subject><ispartof>Life sciences (1973), 2021-02, Vol.267, p.118984, Article 118984</ispartof><rights>2021 Elsevier Inc.</rights><rights>Copyright © 2021 Elsevier Inc. All rights reserved.</rights><rights>Copyright Elsevier BV Feb 15, 2021</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c414t-e48968afe9a5c2360a19e96d805d4f37827542c0759b610c4bf173ba13ea708d3</citedby><cites>FETCH-LOGICAL-c414t-e48968afe9a5c2360a19e96d805d4f37827542c0759b610c4bf173ba13ea708d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0024320520317446$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3536,27903,27904,65309</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33383049$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhan, Chengchuang</creatorcontrib><creatorcontrib>Bai, Nan</creatorcontrib><creatorcontrib>Zheng, Min</creatorcontrib><creatorcontrib>Wang, Yanyan</creatorcontrib><creatorcontrib>Wang, Yuanqi</creatorcontrib><creatorcontrib>Zhang, Li</creatorcontrib><creatorcontrib>Li, Jianqiang</creatorcontrib><creatorcontrib>Li, Guangnan</creatorcontrib><creatorcontrib>Zhao, Hongyan</creatorcontrib><creatorcontrib>Liu, Guangzhong</creatorcontrib><creatorcontrib>Lou, Qi</creatorcontrib><creatorcontrib>Yang, Wen</creatorcontrib><creatorcontrib>Li, Tiankai</creatorcontrib><creatorcontrib>Li, Luyifei</creatorcontrib><creatorcontrib>Li, Weimin</creatorcontrib><title>Tranilast prevents doxorubicin-induced myocardial hypertrophy and angiotensin II synthesis in rats</title><title>Life sciences (1973)</title><addtitle>Life Sci</addtitle><description>An increase in oxidative stress is an important pathological mechanism of heart injury induced by doxorubicin (DOX). Tranilast is an anti-allergy drug that has been shown to possess good antioxidant activity in previous studies. The overexpression and secretion of chymase by mast cells (MCs) increase the pathological overexpression of angiotensin II (Ang II), which plays a crucial role in myocardial hypertrophy and the deterioration of heart disease. The MC stabilizer tranilast (N-(3,4-dimethoxycinnamoyl) anthranilic acid; tran) prevents mast cells from degranulating, which may reduce DOX-induced Ang II synthesis. Therefore, in the present study, we hypothesized that tranilast will protect rats from DOX-induced myocardial damage via its antioxidant activity, thereby inhibiting Ang II expression. Thirty male Wistar rats were divided into three groups (n = 10 in each group) that received DOX, a combination of DOX and tranilast or saline (the control group) to test this hypothesis. Tranilast suppressed chymase expression, reduced Ang II levels and prevented the myocardial hypertrophy and the deterioration of heart function induced by DOX. Based on the findings of the present study, the suppression of chymase-dependent Ang-II production and the direct effect of tranilast on the inhibition of apoptosis and fibrosis because of its antioxidant stress capacity may contribute to the protective effect of tranilast against DOX-induced myocardial hypertrophy.
•Tranilast attenuates the cardiac hypertrophy induced by DOX.•Tranilast prevents the deterioration of heart function induced by DOX.•Tranilast inhibits the expression of Ang II induced by DOX.•Tranilast attenuates oxidative stress and fibrosis induced by DOX.</description><subject>Allergies</subject><subject>Angiotensin</subject><subject>Angiotensin II</subject><subject>Angiotensin II - biosynthesis</subject><subject>Angiotensin II - drug effects</subject><subject>Angiotensin II - metabolism</subject><subject>Animals</subject><subject>Anthranilic acid</subject><subject>antioxidant activity</subject><subject>Antioxidants</subject><subject>Antioxidants - pharmacology</subject><subject>Apoptosis</subject><subject>Cardiomegaly - drug therapy</subject><subject>Cardiomegaly - metabolism</subject><subject>Cardiovascular diseases</subject><subject>Chymase</subject><subject>Coronary artery disease</subject><subject>Deterioration</subject><subject>Doxorubicin</subject><subject>Doxorubicin - adverse effects</subject><subject>Doxorubicin - pharmacology</subject><subject>Fibrosis</subject><subject>heart</subject><subject>Heart diseases</subject><subject>Heart Diseases - etiology</subject><subject>Heart function</subject><subject>Hypertrophy</subject><subject>Male</subject><subject>males</subject><subject>Mast cells</subject><subject>Mast Cells - drug effects</subject><subject>Myocardial hypertrophy</subject><subject>Myocardium - metabolism</subject><subject>ortho-Aminobenzoates - metabolism</subject><subject>ortho-Aminobenzoates - pharmacology</subject><subject>Oxidative stress</subject><subject>Oxidative Stress - drug effects</subject><subject>protective effect</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>secretion</subject><subject>stabilizers</subject><subject>Synthesis</subject><subject>Tranilast</subject><issn>0024-3205</issn><issn>1879-0631</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kU9r3DAQxUVpaLZpP0AuxdBLL96OLMmWyamE_lkI5JKchSyNs1q8kivJof72Vdg0hx5ymBkGfvMY3iPkksKWAm2_HrbTmLYNNGWnspf8DdlQ2fU1tIy-JRuAhtesAXFO3qd0AAAhOvaOnDPGJAPeb8hwF7V3k065miM-os-psuFPiMvgjPO183YxaKvjGoyO1ump2q8zxhzDvF8r7W2pBxcy-uR8tdtVafV5j8mlquxR5_SBnI16SvjxeV6Q-x_f765_1Te3P3fX325qwynPNXLZt1KP2GthGtaCpj32rZUgLB9ZJ5tO8MZAJ_qhpWD4MNKODZoy1B1Iyy7Il5PuHMPvBVNWR5cMTpP2GJakGsFBAMgWCvr5P_QQlujLd4WCtrhXeqHoiTIxpBRxVHN0Rx1XRUE9BaAOqgSgngJQpwDKzadn5WU4on25-Od4Aa5OABYrHh1GlYxDXzx2EU1WNrhX5P8Cld2WWA</recordid><startdate>20210215</startdate><enddate>20210215</enddate><creator>Zhan, Chengchuang</creator><creator>Bai, Nan</creator><creator>Zheng, Min</creator><creator>Wang, Yanyan</creator><creator>Wang, Yuanqi</creator><creator>Zhang, Li</creator><creator>Li, Jianqiang</creator><creator>Li, Guangnan</creator><creator>Zhao, Hongyan</creator><creator>Liu, Guangzhong</creator><creator>Lou, Qi</creator><creator>Yang, Wen</creator><creator>Li, Tiankai</creator><creator>Li, Luyifei</creator><creator>Li, Weimin</creator><general>Elsevier Inc</general><general>Elsevier BV</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>7QP</scope><scope>7QR</scope><scope>7TK</scope><scope>7U7</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>RC3</scope><scope>7S9</scope><scope>L.6</scope></search><sort><creationdate>20210215</creationdate><title>Tranilast prevents doxorubicin-induced myocardial hypertrophy and angiotensin II synthesis in rats</title><author>Zhan, Chengchuang ; Bai, Nan ; Zheng, Min ; Wang, Yanyan ; Wang, Yuanqi ; Zhang, Li ; Li, Jianqiang ; Li, Guangnan ; Zhao, Hongyan ; Liu, Guangzhong ; Lou, Qi ; Yang, Wen ; Li, Tiankai ; Li, Luyifei ; Li, Weimin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c414t-e48968afe9a5c2360a19e96d805d4f37827542c0759b610c4bf173ba13ea708d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Allergies</topic><topic>Angiotensin</topic><topic>Angiotensin II</topic><topic>Angiotensin II - biosynthesis</topic><topic>Angiotensin II - drug effects</topic><topic>Angiotensin II - metabolism</topic><topic>Animals</topic><topic>Anthranilic acid</topic><topic>antioxidant activity</topic><topic>Antioxidants</topic><topic>Antioxidants - pharmacology</topic><topic>Apoptosis</topic><topic>Cardiomegaly - drug therapy</topic><topic>Cardiomegaly - metabolism</topic><topic>Cardiovascular diseases</topic><topic>Chymase</topic><topic>Coronary artery disease</topic><topic>Deterioration</topic><topic>Doxorubicin</topic><topic>Doxorubicin - adverse effects</topic><topic>Doxorubicin - pharmacology</topic><topic>Fibrosis</topic><topic>heart</topic><topic>Heart diseases</topic><topic>Heart Diseases - etiology</topic><topic>Heart function</topic><topic>Hypertrophy</topic><topic>Male</topic><topic>males</topic><topic>Mast cells</topic><topic>Mast Cells - drug effects</topic><topic>Myocardial hypertrophy</topic><topic>Myocardium - metabolism</topic><topic>ortho-Aminobenzoates - metabolism</topic><topic>ortho-Aminobenzoates - pharmacology</topic><topic>Oxidative stress</topic><topic>Oxidative Stress - drug effects</topic><topic>protective effect</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>secretion</topic><topic>stabilizers</topic><topic>Synthesis</topic><topic>Tranilast</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhan, Chengchuang</creatorcontrib><creatorcontrib>Bai, Nan</creatorcontrib><creatorcontrib>Zheng, Min</creatorcontrib><creatorcontrib>Wang, Yanyan</creatorcontrib><creatorcontrib>Wang, Yuanqi</creatorcontrib><creatorcontrib>Zhang, Li</creatorcontrib><creatorcontrib>Li, Jianqiang</creatorcontrib><creatorcontrib>Li, Guangnan</creatorcontrib><creatorcontrib>Zhao, Hongyan</creatorcontrib><creatorcontrib>Liu, Guangzhong</creatorcontrib><creatorcontrib>Lou, Qi</creatorcontrib><creatorcontrib>Yang, Wen</creatorcontrib><creatorcontrib>Li, Tiankai</creatorcontrib><creatorcontrib>Li, Luyifei</creatorcontrib><creatorcontrib>Li, Weimin</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>AGRICOLA</collection><collection>AGRICOLA - Academic</collection><jtitle>Life sciences (1973)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhan, Chengchuang</au><au>Bai, Nan</au><au>Zheng, Min</au><au>Wang, Yanyan</au><au>Wang, Yuanqi</au><au>Zhang, Li</au><au>Li, Jianqiang</au><au>Li, Guangnan</au><au>Zhao, Hongyan</au><au>Liu, Guangzhong</au><au>Lou, Qi</au><au>Yang, Wen</au><au>Li, Tiankai</au><au>Li, Luyifei</au><au>Li, Weimin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Tranilast prevents doxorubicin-induced myocardial hypertrophy and angiotensin II synthesis in rats</atitle><jtitle>Life sciences (1973)</jtitle><addtitle>Life Sci</addtitle><date>2021-02-15</date><risdate>2021</risdate><volume>267</volume><spage>118984</spage><pages>118984-</pages><artnum>118984</artnum><issn>0024-3205</issn><eissn>1879-0631</eissn><abstract>An increase in oxidative stress is an important pathological mechanism of heart injury induced by doxorubicin (DOX). Tranilast is an anti-allergy drug that has been shown to possess good antioxidant activity in previous studies. The overexpression and secretion of chymase by mast cells (MCs) increase the pathological overexpression of angiotensin II (Ang II), which plays a crucial role in myocardial hypertrophy and the deterioration of heart disease. The MC stabilizer tranilast (N-(3,4-dimethoxycinnamoyl) anthranilic acid; tran) prevents mast cells from degranulating, which may reduce DOX-induced Ang II synthesis. Therefore, in the present study, we hypothesized that tranilast will protect rats from DOX-induced myocardial damage via its antioxidant activity, thereby inhibiting Ang II expression. Thirty male Wistar rats were divided into three groups (n = 10 in each group) that received DOX, a combination of DOX and tranilast or saline (the control group) to test this hypothesis. Tranilast suppressed chymase expression, reduced Ang II levels and prevented the myocardial hypertrophy and the deterioration of heart function induced by DOX. Based on the findings of the present study, the suppression of chymase-dependent Ang-II production and the direct effect of tranilast on the inhibition of apoptosis and fibrosis because of its antioxidant stress capacity may contribute to the protective effect of tranilast against DOX-induced myocardial hypertrophy.
•Tranilast attenuates the cardiac hypertrophy induced by DOX.•Tranilast prevents the deterioration of heart function induced by DOX.•Tranilast inhibits the expression of Ang II induced by DOX.•Tranilast attenuates oxidative stress and fibrosis induced by DOX.</abstract><cop>Netherlands</cop><pub>Elsevier Inc</pub><pmid>33383049</pmid><doi>10.1016/j.lfs.2020.118984</doi></addata></record> |
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| subjects | Allergies Angiotensin Angiotensin II Angiotensin II - biosynthesis Angiotensin II - drug effects Angiotensin II - metabolism Animals Anthranilic acid antioxidant activity Antioxidants Antioxidants - pharmacology Apoptosis Cardiomegaly - drug therapy Cardiomegaly - metabolism Cardiovascular diseases Chymase Coronary artery disease Deterioration Doxorubicin Doxorubicin - adverse effects Doxorubicin - pharmacology Fibrosis heart Heart diseases Heart Diseases - etiology Heart function Hypertrophy Male males Mast cells Mast Cells - drug effects Myocardial hypertrophy Myocardium - metabolism ortho-Aminobenzoates - metabolism ortho-Aminobenzoates - pharmacology Oxidative stress Oxidative Stress - drug effects protective effect Rats Rats, Wistar secretion stabilizers Synthesis Tranilast |
| title | Tranilast prevents doxorubicin-induced myocardial hypertrophy and angiotensin II synthesis in rats |
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