Alarin alleviated cardiac fibrosis via attenuating oxidative stress in heart failure rats
The present study was to explore whether alarin could alleviate heart failure (HF) and attenuate cardia fibrosis via inhibiting oxidative stress. The fibrosis of cardiac fibroblasts (CFs) was induced by angiotensin (Ang) II. HF models were induced by ligation of the left anterior descending artery t...
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| Veröffentlicht in: | Amino acids 2021-07, Vol.53 (7), p.1079-1089 |
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| creator | Li, Jinshuang Ding, Hao Li, Yong Zhou, Hao Wang, Wanhong Mei, Yong Zhang, Ronglin |
| description | The present study was to explore whether alarin could alleviate heart failure (HF) and attenuate cardia fibrosis via inhibiting oxidative stress. The fibrosis of cardiac fibroblasts (CFs) was induced by angiotensin (Ang) II. HF models were induced by ligation of the left anterior descending artery to cause ischemia myocardial infarction (MI) in Sprague–Dawley rats. Alarin (1.0 nM/kg/d) was administrated by intraperitoneal injection for 28 days. The decreases of left ventricular (LV) ejection fraction (EF), fractional shortening (FS), the maximum of the first differentiation of LV pressure (LV ± d
p
/d
t
max
) and LV systolic pressure (LVSP), and the increases of LV volume in systole (LVVS), LV volume in diastole (LVVD), LV end-systolic diameter (LVESD) and LV end-diastolic diameter (LVEDD) in MI rats were improved by alarin treatment. The increases in the expression levels of collagen I, collagen III, and transforming growth factor (TGF)-β were inhibited by alarin treatment in CFs and in the hearts of MI rats. The levels of NADPH oxidase (Nox) activity, superoxide anions and malondialdehyde (MDA) levels were increased, and the level of superoxide dismutase (SOD) activity was reduced in Ang II-treated CFs, which were reversed by alarin. Nox1 overexpression reversed the effects of alarin on attenuating the increases of collagen I, collagen III and TGF-β expression levels induced by Ang II in CFs. These results indicated that alarin improved HF and cardiac fibrosis via inhibiting oxidative stress in HF rats. Nox1 played important roles in the regulation of alarin effects on attenuating CFs fibrosis induced by Ang II. |
| doi_str_mv | 10.1007/s00726-021-03005-8 |
| format | Article |
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p
/d
t
max
) and LV systolic pressure (LVSP), and the increases of LV volume in systole (LVVS), LV volume in diastole (LVVD), LV end-systolic diameter (LVESD) and LV end-diastolic diameter (LVEDD) in MI rats were improved by alarin treatment. The increases in the expression levels of collagen I, collagen III, and transforming growth factor (TGF)-β were inhibited by alarin treatment in CFs and in the hearts of MI rats. The levels of NADPH oxidase (Nox) activity, superoxide anions and malondialdehyde (MDA) levels were increased, and the level of superoxide dismutase (SOD) activity was reduced in Ang II-treated CFs, which were reversed by alarin. Nox1 overexpression reversed the effects of alarin on attenuating the increases of collagen I, collagen III and TGF-β expression levels induced by Ang II in CFs. These results indicated that alarin improved HF and cardiac fibrosis via inhibiting oxidative stress in HF rats. Nox1 played important roles in the regulation of alarin effects on attenuating CFs fibrosis induced by Ang II.</description><identifier>ISSN: 0939-4451</identifier><identifier>EISSN: 1438-2199</identifier><identifier>DOI: 10.1007/s00726-021-03005-8</identifier><identifier>PMID: 34089389</identifier><language>eng</language><publisher>Vienna: Springer Vienna</publisher><subject>Analytical Chemistry ; Angiotensin ; Angiotensin II ; Angiotensin II - toxicity ; Animals ; Anions ; Attenuation ; Biochemical Engineering ; Biochemistry ; Biomedical and Life Sciences ; Blood pressure ; Collagen ; Collagen (type I) ; Collagen (type III) ; Congestive heart failure ; Diastole ; Fibroblasts ; Fibrosis ; Fibrosis - etiology ; Fibrosis - pathology ; Fibrosis - prevention & control ; Galanin-Like Peptide - pharmacology ; Growth factors ; Heart failure ; Heart Failure - complications ; Ischemia ; Life Sciences ; Male ; Malondialdehyde ; Malondialdehyde - metabolism ; Myocardial infarction ; Myocardial Infarction - complications ; NAD(P)H oxidase ; Neurobiology ; Original ; Original Article ; Oxidative Stress ; Proteomics ; Rats ; Rats, Sprague-Dawley ; Superoxide anions ; Superoxide dismutase ; Systole ; Systolic pressure ; Transforming Growth Factor beta - metabolism ; Vasoconstrictor Agents - toxicity ; Ventricle</subject><ispartof>Amino acids, 2021-07, Vol.53 (7), p.1079-1089</ispartof><rights>The Author(s) 2021</rights><rights>The Author(s) 2021. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c474t-af9d62bb5a234f1f1827ba6193ffe7573ed58b5ca5cb1f8ea8fa3c631647989d3</citedby><cites>FETCH-LOGICAL-c474t-af9d62bb5a234f1f1827ba6193ffe7573ed58b5ca5cb1f8ea8fa3c631647989d3</cites><orcidid>0000-0001-9643-1769</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00726-021-03005-8$$EPDF$$P50$$Gspringer$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00726-021-03005-8$$EHTML$$P50$$Gspringer$$Hfree_for_read</linktohtml><link.rule.ids>230,314,776,780,881,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34089389$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Li, Jinshuang</creatorcontrib><creatorcontrib>Ding, Hao</creatorcontrib><creatorcontrib>Li, Yong</creatorcontrib><creatorcontrib>Zhou, Hao</creatorcontrib><creatorcontrib>Wang, Wanhong</creatorcontrib><creatorcontrib>Mei, Yong</creatorcontrib><creatorcontrib>Zhang, Ronglin</creatorcontrib><title>Alarin alleviated cardiac fibrosis via attenuating oxidative stress in heart failure rats</title><title>Amino acids</title><addtitle>Amino Acids</addtitle><addtitle>Amino Acids</addtitle><description>The present study was to explore whether alarin could alleviate heart failure (HF) and attenuate cardia fibrosis via inhibiting oxidative stress. The fibrosis of cardiac fibroblasts (CFs) was induced by angiotensin (Ang) II. HF models were induced by ligation of the left anterior descending artery to cause ischemia myocardial infarction (MI) in Sprague–Dawley rats. Alarin (1.0 nM/kg/d) was administrated by intraperitoneal injection for 28 days. The decreases of left ventricular (LV) ejection fraction (EF), fractional shortening (FS), the maximum of the first differentiation of LV pressure (LV ± d
p
/d
t
max
) and LV systolic pressure (LVSP), and the increases of LV volume in systole (LVVS), LV volume in diastole (LVVD), LV end-systolic diameter (LVESD) and LV end-diastolic diameter (LVEDD) in MI rats were improved by alarin treatment. The increases in the expression levels of collagen I, collagen III, and transforming growth factor (TGF)-β were inhibited by alarin treatment in CFs and in the hearts of MI rats. The levels of NADPH oxidase (Nox) activity, superoxide anions and malondialdehyde (MDA) levels were increased, and the level of superoxide dismutase (SOD) activity was reduced in Ang II-treated CFs, which were reversed by alarin. Nox1 overexpression reversed the effects of alarin on attenuating the increases of collagen I, collagen III and TGF-β expression levels induced by Ang II in CFs. These results indicated that alarin improved HF and cardiac fibrosis via inhibiting oxidative stress in HF rats. Nox1 played important roles in the regulation of alarin effects on attenuating CFs fibrosis induced by Ang II.</description><subject>Analytical Chemistry</subject><subject>Angiotensin</subject><subject>Angiotensin II</subject><subject>Angiotensin II - toxicity</subject><subject>Animals</subject><subject>Anions</subject><subject>Attenuation</subject><subject>Biochemical Engineering</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Blood pressure</subject><subject>Collagen</subject><subject>Collagen (type I)</subject><subject>Collagen (type III)</subject><subject>Congestive heart failure</subject><subject>Diastole</subject><subject>Fibroblasts</subject><subject>Fibrosis</subject><subject>Fibrosis - etiology</subject><subject>Fibrosis - pathology</subject><subject>Fibrosis - prevention & control</subject><subject>Galanin-Like Peptide - pharmacology</subject><subject>Growth factors</subject><subject>Heart failure</subject><subject>Heart Failure - complications</subject><subject>Ischemia</subject><subject>Life Sciences</subject><subject>Male</subject><subject>Malondialdehyde</subject><subject>Malondialdehyde - metabolism</subject><subject>Myocardial infarction</subject><subject>Myocardial Infarction - complications</subject><subject>NAD(P)H oxidase</subject><subject>Neurobiology</subject><subject>Original</subject><subject>Original Article</subject><subject>Oxidative Stress</subject><subject>Proteomics</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Superoxide anions</subject><subject>Superoxide dismutase</subject><subject>Systole</subject><subject>Systolic pressure</subject><subject>Transforming Growth Factor beta - metabolism</subject><subject>Vasoconstrictor Agents - toxicity</subject><subject>Ventricle</subject><issn>0939-4451</issn><issn>1438-2199</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp9kbtuFTEQhi0EIofAC1AgSzQ0S3y_NEhRxE2KlAYKKmt2d3ziaM9usL1H8PY4nBAIRRqP5fnmH8_8hLzk7C1nzJ6UdgjTMcE7JhnTnXtENlxJ1wnu_WOyYV76TinNj8izUq4Y48Jx85QcScWcl85vyLfTCXKaKUwT7hNUHOkAeUww0Jj6vJRUaHunUCvOK9Q0b-nyI43ttkdaasZSaKu_RMiVRkjTmpFmqOU5eRJhKvjiNh6Trx_efzn71J1ffPx8dnreDcqq2kH0oxF9r0FIFXnkTtgeDPcyRrTaShy16_UAeuh5dAgughyM5EZZ7_woj8m7g-712u9wHHCuGaZwndMO8s-wQAr3M3O6DNtlH5xQ3HrbBN7cCuTl-4qlhl0qA04TzLisJQgtrVHaGtfQ1_-hV8ua5zZeo5SR3kkjGiUO1ND2VzLGu89wFm6cCwfnQnMu_HYu3Ei_-neMu5I_VjVAHoDSUvMW89_eD8j-AunNph4</recordid><startdate>20210701</startdate><enddate>20210701</enddate><creator>Li, Jinshuang</creator><creator>Ding, Hao</creator><creator>Li, Yong</creator><creator>Zhou, Hao</creator><creator>Wang, Wanhong</creator><creator>Mei, Yong</creator><creator>Zhang, Ronglin</creator><general>Springer Vienna</general><general>Springer Nature B.V</general><scope>C6C</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>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>PDBOC</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0001-9643-1769</orcidid></search><sort><creationdate>20210701</creationdate><title>Alarin alleviated cardiac fibrosis via attenuating oxidative stress in heart failure rats</title><author>Li, Jinshuang ; Ding, Hao ; Li, Yong ; Zhou, Hao ; Wang, Wanhong ; Mei, Yong ; Zhang, Ronglin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c474t-af9d62bb5a234f1f1827ba6193ffe7573ed58b5ca5cb1f8ea8fa3c631647989d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Analytical Chemistry</topic><topic>Angiotensin</topic><topic>Angiotensin II</topic><topic>Angiotensin II - toxicity</topic><topic>Animals</topic><topic>Anions</topic><topic>Attenuation</topic><topic>Biochemical Engineering</topic><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Blood pressure</topic><topic>Collagen</topic><topic>Collagen (type I)</topic><topic>Collagen (type III)</topic><topic>Congestive heart failure</topic><topic>Diastole</topic><topic>Fibroblasts</topic><topic>Fibrosis</topic><topic>Fibrosis - etiology</topic><topic>Fibrosis - pathology</topic><topic>Fibrosis - prevention & control</topic><topic>Galanin-Like Peptide - pharmacology</topic><topic>Growth factors</topic><topic>Heart failure</topic><topic>Heart Failure - complications</topic><topic>Ischemia</topic><topic>Life Sciences</topic><topic>Male</topic><topic>Malondialdehyde</topic><topic>Malondialdehyde - metabolism</topic><topic>Myocardial infarction</topic><topic>Myocardial Infarction - complications</topic><topic>NAD(P)H oxidase</topic><topic>Neurobiology</topic><topic>Original</topic><topic>Original Article</topic><topic>Oxidative Stress</topic><topic>Proteomics</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Superoxide anions</topic><topic>Superoxide dismutase</topic><topic>Systole</topic><topic>Systolic pressure</topic><topic>Transforming Growth Factor beta - metabolism</topic><topic>Vasoconstrictor Agents - toxicity</topic><topic>Ventricle</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Li, Jinshuang</creatorcontrib><creatorcontrib>Ding, Hao</creatorcontrib><creatorcontrib>Li, Yong</creatorcontrib><creatorcontrib>Zhou, Hao</creatorcontrib><creatorcontrib>Wang, Wanhong</creatorcontrib><creatorcontrib>Mei, Yong</creatorcontrib><creatorcontrib>Zhang, Ronglin</creatorcontrib><collection>Springer Nature OA Free Journals</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Materials Science Collection</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Materials Science Database</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Materials Science Collection</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Amino acids</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Li, Jinshuang</au><au>Ding, Hao</au><au>Li, Yong</au><au>Zhou, Hao</au><au>Wang, Wanhong</au><au>Mei, Yong</au><au>Zhang, Ronglin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Alarin alleviated cardiac fibrosis via attenuating oxidative stress in heart failure rats</atitle><jtitle>Amino acids</jtitle><stitle>Amino Acids</stitle><addtitle>Amino Acids</addtitle><date>2021-07-01</date><risdate>2021</risdate><volume>53</volume><issue>7</issue><spage>1079</spage><epage>1089</epage><pages>1079-1089</pages><issn>0939-4451</issn><eissn>1438-2199</eissn><abstract>The present study was to explore whether alarin could alleviate heart failure (HF) and attenuate cardia fibrosis via inhibiting oxidative stress. The fibrosis of cardiac fibroblasts (CFs) was induced by angiotensin (Ang) II. HF models were induced by ligation of the left anterior descending artery to cause ischemia myocardial infarction (MI) in Sprague–Dawley rats. Alarin (1.0 nM/kg/d) was administrated by intraperitoneal injection for 28 days. The decreases of left ventricular (LV) ejection fraction (EF), fractional shortening (FS), the maximum of the first differentiation of LV pressure (LV ± d
p
/d
t
max
) and LV systolic pressure (LVSP), and the increases of LV volume in systole (LVVS), LV volume in diastole (LVVD), LV end-systolic diameter (LVESD) and LV end-diastolic diameter (LVEDD) in MI rats were improved by alarin treatment. The increases in the expression levels of collagen I, collagen III, and transforming growth factor (TGF)-β were inhibited by alarin treatment in CFs and in the hearts of MI rats. The levels of NADPH oxidase (Nox) activity, superoxide anions and malondialdehyde (MDA) levels were increased, and the level of superoxide dismutase (SOD) activity was reduced in Ang II-treated CFs, which were reversed by alarin. Nox1 overexpression reversed the effects of alarin on attenuating the increases of collagen I, collagen III and TGF-β expression levels induced by Ang II in CFs. These results indicated that alarin improved HF and cardiac fibrosis via inhibiting oxidative stress in HF rats. Nox1 played important roles in the regulation of alarin effects on attenuating CFs fibrosis induced by Ang II.</abstract><cop>Vienna</cop><pub>Springer Vienna</pub><pmid>34089389</pmid><doi>10.1007/s00726-021-03005-8</doi><tpages>11</tpages><orcidid>https://orcid.org/0000-0001-9643-1769</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Analytical Chemistry Angiotensin Angiotensin II Angiotensin II - toxicity Animals Anions Attenuation Biochemical Engineering Biochemistry Biomedical and Life Sciences Blood pressure Collagen Collagen (type I) Collagen (type III) Congestive heart failure Diastole Fibroblasts Fibrosis Fibrosis - etiology Fibrosis - pathology Fibrosis - prevention & control Galanin-Like Peptide - pharmacology Growth factors Heart failure Heart Failure - complications Ischemia Life Sciences Male Malondialdehyde Malondialdehyde - metabolism Myocardial infarction Myocardial Infarction - complications NAD(P)H oxidase Neurobiology Original Original Article Oxidative Stress Proteomics Rats Rats, Sprague-Dawley Superoxide anions Superoxide dismutase Systole Systolic pressure Transforming Growth Factor beta - metabolism Vasoconstrictor Agents - toxicity Ventricle |
| title | Alarin alleviated cardiac fibrosis via attenuating oxidative stress in heart failure rats |
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