Hesperetin ameliorates ischemia/hypoxia‐induced myocardium injury via inhibition of oxidative stress, apoptosis, and regulation of Ca2+ homeostasis
Ischemia/hypoxia (I/H)‐induced myocardial injury has a large burden worldwide. Hesperetin (HSP) has a cardioprotective effect, but the molecular mechanism underlying this is not clearly established. Here, we focused on the protective mechanisms of HSP against I/H‐induced myocardium injury. H9c2 card...
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| Veröffentlicht in: | Phytotherapy research 2023-05, Vol.37 (5), p.1787-1805 |
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| creator | Liu, Panpan Chen, Jian Qi, Jiaying Liu, Miaomiao Zhang, Muqing Xue, Yucong Li, Li Liu, Yanshuang Shi, Jing Zhang, Yixin Chu, Li |
| description | Ischemia/hypoxia (I/H)‐induced myocardial injury has a large burden worldwide. Hesperetin (HSP) has a cardioprotective effect, but the molecular mechanism underlying this is not clearly established. Here, we focused on the protective mechanisms of HSP against I/H‐induced myocardium injury. H9c2 cardiomyocytes were challenged with CoCl2 for 22 h to imitate hypoxia after treatment groups received HSP for 4 h. The viability of H9c2 cardiomyocytes was evaluated, and cardiac function indices, reactive oxygen species, apoptosis, mitochondrial membrane potential (MMP), and intracellular Ca2+ concentration ([Ca2+]i) were measured. L‐type Ca2+ current (ICa‐L), myocardial contraction, and Ca2+ transients in isolated ventricular myocytes were also recorded. We found that HSP significantly increased the cell viability, and MMP while significantly decreasing cardiac impairment, oxidative stress, apoptosis, and [Ca2+]i caused by CoCl2. Furthermore, HSP markedly attenuated ICa‐L, myocardial contraction, and Ca2+ transients in a concentration‐dependent manner. Our findings suggest a protective mechanism of HSP on I/H‐induced myocardium injury by restoring oxidative balance, inhibiting apoptosis, improving mitochondrial function, and reducing Ca2+ influx via L‐type Ca2+ channels (LTCCs). These data provide a new direction for HSP applied research as a LTCC inhibitor against I/H‐induced myocardium injury. |
| doi_str_mv | 10.1002/ptr.7693 |
| format | Article |
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Hesperetin (HSP) has a cardioprotective effect, but the molecular mechanism underlying this is not clearly established. Here, we focused on the protective mechanisms of HSP against I/H‐induced myocardium injury. H9c2 cardiomyocytes were challenged with CoCl2 for 22 h to imitate hypoxia after treatment groups received HSP for 4 h. The viability of H9c2 cardiomyocytes was evaluated, and cardiac function indices, reactive oxygen species, apoptosis, mitochondrial membrane potential (MMP), and intracellular Ca2+ concentration ([Ca2+]i) were measured. L‐type Ca2+ current (ICa‐L), myocardial contraction, and Ca2+ transients in isolated ventricular myocytes were also recorded. We found that HSP significantly increased the cell viability, and MMP while significantly decreasing cardiac impairment, oxidative stress, apoptosis, and [Ca2+]i caused by CoCl2. Furthermore, HSP markedly attenuated ICa‐L, myocardial contraction, and Ca2+ transients in a concentration‐dependent manner. Our findings suggest a protective mechanism of HSP on I/H‐induced myocardium injury by restoring oxidative balance, inhibiting apoptosis, improving mitochondrial function, and reducing Ca2+ influx via L‐type Ca2+ channels (LTCCs). These data provide a new direction for HSP applied research as a LTCC inhibitor against I/H‐induced myocardium injury.</description><identifier>ISSN: 0951-418X</identifier><identifier>EISSN: 1099-1573</identifier><identifier>DOI: 10.1002/ptr.7693</identifier><language>eng</language><publisher>Chichester, UK: John Wiley & Sons, Ltd</publisher><subject>Apoptosis ; Calcium (intracellular) ; Calcium (mitochondrial) ; Calcium channels ; Calcium homeostasis ; Calcium influx ; Calcium ions ; Cardiac muscle ; Cardiomyocytes ; Cell viability ; Heart ; Heart function ; hesperetin ; Hesperidin ; Homeostasis ; Hypoxia ; Injuries ; Ischemia ; L‐type Ca2+ channels ; Membrane potential ; Mitochondria ; Molecular modelling ; myocardial contraction ; myocardial ischemia/hypoxia ; Myocardium ; Myocytes ; Oxidative stress ; Reactive oxygen species ; Ventricle</subject><ispartof>Phytotherapy research, 2023-05, Vol.37 (5), p.1787-1805</ispartof><rights>2022 John Wiley & Sons Ltd.</rights><rights>2023 John Wiley & Sons, Ltd.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><orcidid>0000-0002-6301-2709</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fptr.7693$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fptr.7693$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids></links><search><creatorcontrib>Liu, Panpan</creatorcontrib><creatorcontrib>Chen, Jian</creatorcontrib><creatorcontrib>Qi, Jiaying</creatorcontrib><creatorcontrib>Liu, Miaomiao</creatorcontrib><creatorcontrib>Zhang, Muqing</creatorcontrib><creatorcontrib>Xue, Yucong</creatorcontrib><creatorcontrib>Li, Li</creatorcontrib><creatorcontrib>Liu, Yanshuang</creatorcontrib><creatorcontrib>Shi, Jing</creatorcontrib><creatorcontrib>Zhang, Yixin</creatorcontrib><creatorcontrib>Chu, Li</creatorcontrib><title>Hesperetin ameliorates ischemia/hypoxia‐induced myocardium injury via inhibition of oxidative stress, apoptosis, and regulation of Ca2+ homeostasis</title><title>Phytotherapy research</title><description>Ischemia/hypoxia (I/H)‐induced myocardial injury has a large burden worldwide. Hesperetin (HSP) has a cardioprotective effect, but the molecular mechanism underlying this is not clearly established. Here, we focused on the protective mechanisms of HSP against I/H‐induced myocardium injury. H9c2 cardiomyocytes were challenged with CoCl2 for 22 h to imitate hypoxia after treatment groups received HSP for 4 h. The viability of H9c2 cardiomyocytes was evaluated, and cardiac function indices, reactive oxygen species, apoptosis, mitochondrial membrane potential (MMP), and intracellular Ca2+ concentration ([Ca2+]i) were measured. L‐type Ca2+ current (ICa‐L), myocardial contraction, and Ca2+ transients in isolated ventricular myocytes were also recorded. We found that HSP significantly increased the cell viability, and MMP while significantly decreasing cardiac impairment, oxidative stress, apoptosis, and [Ca2+]i caused by CoCl2. Furthermore, HSP markedly attenuated ICa‐L, myocardial contraction, and Ca2+ transients in a concentration‐dependent manner. Our findings suggest a protective mechanism of HSP on I/H‐induced myocardium injury by restoring oxidative balance, inhibiting apoptosis, improving mitochondrial function, and reducing Ca2+ influx via L‐type Ca2+ channels (LTCCs). These data provide a new direction for HSP applied research as a LTCC inhibitor against I/H‐induced myocardium injury.</description><subject>Apoptosis</subject><subject>Calcium (intracellular)</subject><subject>Calcium (mitochondrial)</subject><subject>Calcium channels</subject><subject>Calcium homeostasis</subject><subject>Calcium influx</subject><subject>Calcium ions</subject><subject>Cardiac muscle</subject><subject>Cardiomyocytes</subject><subject>Cell viability</subject><subject>Heart</subject><subject>Heart function</subject><subject>hesperetin</subject><subject>Hesperidin</subject><subject>Homeostasis</subject><subject>Hypoxia</subject><subject>Injuries</subject><subject>Ischemia</subject><subject>L‐type Ca2+ channels</subject><subject>Membrane potential</subject><subject>Mitochondria</subject><subject>Molecular modelling</subject><subject>myocardial contraction</subject><subject>myocardial ischemia/hypoxia</subject><subject>Myocardium</subject><subject>Myocytes</subject><subject>Oxidative stress</subject><subject>Reactive oxygen species</subject><subject>Ventricle</subject><issn>0951-418X</issn><issn>1099-1573</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><recordid>eNpdkc-K1EAQhxtRcFwFH6HBi6DZrf6TSfoog7rCgiIreGtq0hWnhyQduzurufkIe9kX9EnsYfXi6fc7fFVU8TH2XMC5AJAXc47nzdaoB2wjwJhK1I16yDZgalFp0X59zJ6kdAQAI0Fv2N0lpZkiZT9xHGnwIWKmxH3qDjR6vDisc_jp8fevWz-5pSPHxzV0GJ1fRu6n4xJXfuOx1IPf--zDxEPPy4jD7G-Ipxwppdcc5zDnkPypTo5H-rYM-A_foXzFD2GkkDIW5il71OOQ6NnfPGNf3r293l1WVx_ff9i9uapm0WpVddD3KNutAr1FJakRCEIpkrWRqnZa7Alb6KTRomDGKd3W2jTaKXB71Rt1xl7e751j-L5QynYsj9Mw4ERhSVY2GgxstYSCvvgPPYYlTuU6K1shtGpaUIWq7qkffqDVztGPGFcrwJ7k2CLHnuTYT9efT6n-AI_khxo</recordid><startdate>202305</startdate><enddate>202305</enddate><creator>Liu, Panpan</creator><creator>Chen, Jian</creator><creator>Qi, Jiaying</creator><creator>Liu, Miaomiao</creator><creator>Zhang, Muqing</creator><creator>Xue, Yucong</creator><creator>Li, Li</creator><creator>Liu, Yanshuang</creator><creator>Shi, Jing</creator><creator>Zhang, Yixin</creator><creator>Chu, Li</creator><general>John Wiley & Sons, Ltd</general><general>Wiley Subscription Services, Inc</general><scope>7QO</scope><scope>7QP</scope><scope>7QR</scope><scope>7TK</scope><scope>7TM</scope><scope>8FD</scope><scope>FR3</scope><scope>K9.</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-6301-2709</orcidid></search><sort><creationdate>202305</creationdate><title>Hesperetin ameliorates ischemia/hypoxia‐induced myocardium injury via inhibition of oxidative stress, apoptosis, and regulation of Ca2+ homeostasis</title><author>Liu, Panpan ; Chen, Jian ; Qi, Jiaying ; Liu, Miaomiao ; Zhang, Muqing ; Xue, Yucong ; Li, Li ; Liu, Yanshuang ; Shi, Jing ; Zhang, Yixin ; Chu, Li</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p1843-c0ffa2863046a32e71a0133e259235d41bea80c2941a289d34854974d30db3f93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Apoptosis</topic><topic>Calcium (intracellular)</topic><topic>Calcium (mitochondrial)</topic><topic>Calcium channels</topic><topic>Calcium homeostasis</topic><topic>Calcium influx</topic><topic>Calcium ions</topic><topic>Cardiac muscle</topic><topic>Cardiomyocytes</topic><topic>Cell viability</topic><topic>Heart</topic><topic>Heart function</topic><topic>hesperetin</topic><topic>Hesperidin</topic><topic>Homeostasis</topic><topic>Hypoxia</topic><topic>Injuries</topic><topic>Ischemia</topic><topic>L‐type Ca2+ channels</topic><topic>Membrane potential</topic><topic>Mitochondria</topic><topic>Molecular modelling</topic><topic>myocardial contraction</topic><topic>myocardial ischemia/hypoxia</topic><topic>Myocardium</topic><topic>Myocytes</topic><topic>Oxidative stress</topic><topic>Reactive oxygen species</topic><topic>Ventricle</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Liu, Panpan</creatorcontrib><creatorcontrib>Chen, Jian</creatorcontrib><creatorcontrib>Qi, Jiaying</creatorcontrib><creatorcontrib>Liu, Miaomiao</creatorcontrib><creatorcontrib>Zhang, Muqing</creatorcontrib><creatorcontrib>Xue, Yucong</creatorcontrib><creatorcontrib>Li, Li</creatorcontrib><creatorcontrib>Liu, Yanshuang</creatorcontrib><creatorcontrib>Shi, Jing</creatorcontrib><creatorcontrib>Zhang, Yixin</creatorcontrib><creatorcontrib>Chu, Li</creatorcontrib><collection>Biotechnology Research Abstracts</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Phytotherapy research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Liu, Panpan</au><au>Chen, Jian</au><au>Qi, Jiaying</au><au>Liu, Miaomiao</au><au>Zhang, Muqing</au><au>Xue, Yucong</au><au>Li, Li</au><au>Liu, Yanshuang</au><au>Shi, Jing</au><au>Zhang, Yixin</au><au>Chu, Li</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Hesperetin ameliorates ischemia/hypoxia‐induced myocardium injury via inhibition of oxidative stress, apoptosis, and regulation of Ca2+ homeostasis</atitle><jtitle>Phytotherapy research</jtitle><date>2023-05</date><risdate>2023</risdate><volume>37</volume><issue>5</issue><spage>1787</spage><epage>1805</epage><pages>1787-1805</pages><issn>0951-418X</issn><eissn>1099-1573</eissn><abstract>Ischemia/hypoxia (I/H)‐induced myocardial injury has a large burden worldwide. Hesperetin (HSP) has a cardioprotective effect, but the molecular mechanism underlying this is not clearly established. Here, we focused on the protective mechanisms of HSP against I/H‐induced myocardium injury. H9c2 cardiomyocytes were challenged with CoCl2 for 22 h to imitate hypoxia after treatment groups received HSP for 4 h. The viability of H9c2 cardiomyocytes was evaluated, and cardiac function indices, reactive oxygen species, apoptosis, mitochondrial membrane potential (MMP), and intracellular Ca2+ concentration ([Ca2+]i) were measured. L‐type Ca2+ current (ICa‐L), myocardial contraction, and Ca2+ transients in isolated ventricular myocytes were also recorded. We found that HSP significantly increased the cell viability, and MMP while significantly decreasing cardiac impairment, oxidative stress, apoptosis, and [Ca2+]i caused by CoCl2. Furthermore, HSP markedly attenuated ICa‐L, myocardial contraction, and Ca2+ transients in a concentration‐dependent manner. Our findings suggest a protective mechanism of HSP on I/H‐induced myocardium injury by restoring oxidative balance, inhibiting apoptosis, improving mitochondrial function, and reducing Ca2+ influx via L‐type Ca2+ channels (LTCCs). These data provide a new direction for HSP applied research as a LTCC inhibitor against I/H‐induced myocardium injury.</abstract><cop>Chichester, UK</cop><pub>John Wiley & Sons, Ltd</pub><doi>10.1002/ptr.7693</doi><tpages>19</tpages><orcidid>https://orcid.org/0000-0002-6301-2709</orcidid></addata></record> |
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| subjects | Apoptosis Calcium (intracellular) Calcium (mitochondrial) Calcium channels Calcium homeostasis Calcium influx Calcium ions Cardiac muscle Cardiomyocytes Cell viability Heart Heart function hesperetin Hesperidin Homeostasis Hypoxia Injuries Ischemia L‐type Ca2+ channels Membrane potential Mitochondria Molecular modelling myocardial contraction myocardial ischemia/hypoxia Myocardium Myocytes Oxidative stress Reactive oxygen species Ventricle |
| title | Hesperetin ameliorates ischemia/hypoxia‐induced myocardium injury via inhibition of oxidative stress, apoptosis, and regulation of Ca2+ homeostasis |
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