Hyperoside protects against hypoxia/reoxygenation induced injury in cardiomyocytes by suppressing the Bnip3 expression
Role of hyperoside in protecting cardiomyocytes from ischemia/reperfusion induced injury has been proved. However, possible protecting mechanisms remain unclear. To fix the problem, an essential pro-apoptotic protein Bnip3 was studied in our experiments. Neonatal rat cardiomyocytes were used and sub...
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| Veröffentlicht in: | Gene 2017-09, Vol.629, p.86-91 |
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| creator | Xiao, Rui Xiang, An-Li Pang, Hong-Bo Liu, Ke-Qiang |
| description | Role of hyperoside in protecting cardiomyocytes from ischemia/reperfusion induced injury has been proved. However, possible protecting mechanisms remain unclear. To fix the problem, an essential pro-apoptotic protein Bnip3 was studied in our experiments.
Neonatal rat cardiomyocytes were used and submitted to hypoxia for 8h followed by reoxygenation for 2h to simulate the ischemia/reperfusion injury. Hypoxia/reoxygenation(H/R) induced damage to cardiomyocytes and the protective effect of hyperoside were examined by means of MTT assay. H/R-induced apoptosis was assessed by Terminal-deoxynucleoitidyl Transferase Mediated Nick End Labeling(TUNEL) and DNA Ladder assay. mRNA expression of Bnip3 was determined by use of quantitative real-time reverse transcription polymerase chain reaction assay. Protein levels of Bnip3, Bax, Bcl-2 and cleaved caspase-3 were examined using western-blot assay. Our results showed that H/R caused great damage to cardiomyocytes, upregulated the protein expressions of Bnip3, Bax, cleaved caspase3, and decreased the expression of the anti-apoptotic protein of Bcl-2. Whereas, compared with the H/R group, a decrease in activities of Bnip3, Bax, cleaved caspase3, and a promoting expression of Bcl-2 were detected in the H/R goup pretreated with hyperoside.
It was concluded in our study that H/R-induced apoptotic effect in cardiomyocytes could be attenuated by hyperoside, and the protective role of hyperoside, if not completely, could be partly through the suppression of the pro-apoptotic gene Bnip3.
•H/R-induced apoptotic effect in cardiomyocytes.•Hyperoside has a protective role in cardiomyocyte apoptosis.•Hyperoside suppress the expression of Bnip3. |
| doi_str_mv | 10.1016/j.gene.2017.07.063 |
| format | Article |
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Neonatal rat cardiomyocytes were used and submitted to hypoxia for 8h followed by reoxygenation for 2h to simulate the ischemia/reperfusion injury. Hypoxia/reoxygenation(H/R) induced damage to cardiomyocytes and the protective effect of hyperoside were examined by means of MTT assay. H/R-induced apoptosis was assessed by Terminal-deoxynucleoitidyl Transferase Mediated Nick End Labeling(TUNEL) and DNA Ladder assay. mRNA expression of Bnip3 was determined by use of quantitative real-time reverse transcription polymerase chain reaction assay. Protein levels of Bnip3, Bax, Bcl-2 and cleaved caspase-3 were examined using western-blot assay. Our results showed that H/R caused great damage to cardiomyocytes, upregulated the protein expressions of Bnip3, Bax, cleaved caspase3, and decreased the expression of the anti-apoptotic protein of Bcl-2. Whereas, compared with the H/R group, a decrease in activities of Bnip3, Bax, cleaved caspase3, and a promoting expression of Bcl-2 were detected in the H/R goup pretreated with hyperoside.
It was concluded in our study that H/R-induced apoptotic effect in cardiomyocytes could be attenuated by hyperoside, and the protective role of hyperoside, if not completely, could be partly through the suppression of the pro-apoptotic gene Bnip3.
•H/R-induced apoptotic effect in cardiomyocytes.•Hyperoside has a protective role in cardiomyocyte apoptosis.•Hyperoside suppress the expression of Bnip3.</description><identifier>ISSN: 0378-1119</identifier><identifier>EISSN: 1879-0038</identifier><identifier>DOI: 10.1016/j.gene.2017.07.063</identifier><identifier>PMID: 28754633</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>Animals ; Apoptosis ; Bnip3 ; Cardiotonic Agents - pharmacology ; Hyperoside ; Hypoxia/reoxygenation ; Membrane Proteins - genetics ; Membrane Proteins - metabolism ; Mitochondrial Proteins - genetics ; Mitochondrial Proteins - metabolism ; Myocardial Infarction - metabolism ; Myocardial Infarction - pathology ; Myocytes, Cardiac - drug effects ; Myocytes, Cardiac - metabolism ; Myocytes, Cardiac - pathology ; Plants, Medicinal - chemistry ; Quercetin - analogs & derivatives ; Quercetin - pharmacology ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury - metabolism ; Reperfusion Injury - pathology</subject><ispartof>Gene, 2017-09, Vol.629, p.86-91</ispartof><rights>2017 Elsevier B.V.</rights><rights>Copyright © 2017 Elsevier B.V. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c356t-118c7bee4dddabda63a0266a82f5afc30081d7cdab849b83a883de628d9e8c043</citedby><cites>FETCH-LOGICAL-c356t-118c7bee4dddabda63a0266a82f5afc30081d7cdab849b83a883de628d9e8c043</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.gene.2017.07.063$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28754633$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Xiao, Rui</creatorcontrib><creatorcontrib>Xiang, An-Li</creatorcontrib><creatorcontrib>Pang, Hong-Bo</creatorcontrib><creatorcontrib>Liu, Ke-Qiang</creatorcontrib><title>Hyperoside protects against hypoxia/reoxygenation induced injury in cardiomyocytes by suppressing the Bnip3 expression</title><title>Gene</title><addtitle>Gene</addtitle><description>Role of hyperoside in protecting cardiomyocytes from ischemia/reperfusion induced injury has been proved. However, possible protecting mechanisms remain unclear. To fix the problem, an essential pro-apoptotic protein Bnip3 was studied in our experiments.
Neonatal rat cardiomyocytes were used and submitted to hypoxia for 8h followed by reoxygenation for 2h to simulate the ischemia/reperfusion injury. Hypoxia/reoxygenation(H/R) induced damage to cardiomyocytes and the protective effect of hyperoside were examined by means of MTT assay. H/R-induced apoptosis was assessed by Terminal-deoxynucleoitidyl Transferase Mediated Nick End Labeling(TUNEL) and DNA Ladder assay. mRNA expression of Bnip3 was determined by use of quantitative real-time reverse transcription polymerase chain reaction assay. Protein levels of Bnip3, Bax, Bcl-2 and cleaved caspase-3 were examined using western-blot assay. Our results showed that H/R caused great damage to cardiomyocytes, upregulated the protein expressions of Bnip3, Bax, cleaved caspase3, and decreased the expression of the anti-apoptotic protein of Bcl-2. Whereas, compared with the H/R group, a decrease in activities of Bnip3, Bax, cleaved caspase3, and a promoting expression of Bcl-2 were detected in the H/R goup pretreated with hyperoside.
It was concluded in our study that H/R-induced apoptotic effect in cardiomyocytes could be attenuated by hyperoside, and the protective role of hyperoside, if not completely, could be partly through the suppression of the pro-apoptotic gene Bnip3.
•H/R-induced apoptotic effect in cardiomyocytes.•Hyperoside has a protective role in cardiomyocyte apoptosis.•Hyperoside suppress the expression of Bnip3.</description><subject>Animals</subject><subject>Apoptosis</subject><subject>Bnip3</subject><subject>Cardiotonic Agents - pharmacology</subject><subject>Hyperoside</subject><subject>Hypoxia/reoxygenation</subject><subject>Membrane Proteins - genetics</subject><subject>Membrane Proteins - metabolism</subject><subject>Mitochondrial Proteins - genetics</subject><subject>Mitochondrial Proteins - metabolism</subject><subject>Myocardial Infarction - metabolism</subject><subject>Myocardial Infarction - pathology</subject><subject>Myocytes, Cardiac - drug effects</subject><subject>Myocytes, Cardiac - metabolism</subject><subject>Myocytes, Cardiac - pathology</subject><subject>Plants, Medicinal - chemistry</subject><subject>Quercetin - analogs & derivatives</subject><subject>Quercetin - pharmacology</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Reperfusion Injury - metabolism</subject><subject>Reperfusion Injury - pathology</subject><issn>0378-1119</issn><issn>1879-0038</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kE9PAyEQxYnR2Fr9Ah4MRy9tYdll2cSLNv5LmnjRM2Fh2tK0sMJu0_320rR6lEzyEubxmPkhdEvJhBLKp-vJEhxMMkLLCUnF2RkaUlFWY0KYOEdDwkoxppRWA3QV45qkUxTZJRpkoixyztgQ7d76BoKP1gBugm9BtxGrpbIutnjVN35v1TSA3_fpL9Va77B1ptNgkq670CfBWgVj_bb3um8h4rrHsWuaADFat8TtCvCTsw3DsD9eeneNLhZqE-HmpCP09fL8OXsbzz9e32eP87FmBW_T7EKXNUBujFG1UZwpknGuRLYo1EIzQgQ1pU49kVe1YEoIZoBnwlQgNMnZCN0fc9Nu3x3EVm5t1LDZKAe-i5JWWV5UvOI8WbOjVSccMcBCNsFuVeglJfLAW67lgbc88JYkVQI4Qnen_K7egvl78gs4GR6OBkhb7iwEGbUFl_jZkFhL4-1_-T82oZWv</recordid><startdate>20170920</startdate><enddate>20170920</enddate><creator>Xiao, Rui</creator><creator>Xiang, An-Li</creator><creator>Pang, Hong-Bo</creator><creator>Liu, Ke-Qiang</creator><general>Elsevier B.V</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>7X8</scope></search><sort><creationdate>20170920</creationdate><title>Hyperoside protects against hypoxia/reoxygenation induced injury in cardiomyocytes by suppressing the Bnip3 expression</title><author>Xiao, Rui ; Xiang, An-Li ; Pang, Hong-Bo ; Liu, Ke-Qiang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c356t-118c7bee4dddabda63a0266a82f5afc30081d7cdab849b83a883de628d9e8c043</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Animals</topic><topic>Apoptosis</topic><topic>Bnip3</topic><topic>Cardiotonic Agents - pharmacology</topic><topic>Hyperoside</topic><topic>Hypoxia/reoxygenation</topic><topic>Membrane Proteins - genetics</topic><topic>Membrane Proteins - metabolism</topic><topic>Mitochondrial Proteins - genetics</topic><topic>Mitochondrial Proteins - metabolism</topic><topic>Myocardial Infarction - metabolism</topic><topic>Myocardial Infarction - pathology</topic><topic>Myocytes, Cardiac - drug effects</topic><topic>Myocytes, Cardiac - metabolism</topic><topic>Myocytes, Cardiac - pathology</topic><topic>Plants, Medicinal - chemistry</topic><topic>Quercetin - analogs & derivatives</topic><topic>Quercetin - pharmacology</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Reperfusion Injury - metabolism</topic><topic>Reperfusion Injury - pathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Xiao, Rui</creatorcontrib><creatorcontrib>Xiang, An-Li</creatorcontrib><creatorcontrib>Pang, Hong-Bo</creatorcontrib><creatorcontrib>Liu, Ke-Qiang</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><jtitle>Gene</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Xiao, Rui</au><au>Xiang, An-Li</au><au>Pang, Hong-Bo</au><au>Liu, Ke-Qiang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Hyperoside protects against hypoxia/reoxygenation induced injury in cardiomyocytes by suppressing the Bnip3 expression</atitle><jtitle>Gene</jtitle><addtitle>Gene</addtitle><date>2017-09-20</date><risdate>2017</risdate><volume>629</volume><spage>86</spage><epage>91</epage><pages>86-91</pages><issn>0378-1119</issn><eissn>1879-0038</eissn><abstract>Role of hyperoside in protecting cardiomyocytes from ischemia/reperfusion induced injury has been proved. However, possible protecting mechanisms remain unclear. To fix the problem, an essential pro-apoptotic protein Bnip3 was studied in our experiments.
Neonatal rat cardiomyocytes were used and submitted to hypoxia for 8h followed by reoxygenation for 2h to simulate the ischemia/reperfusion injury. Hypoxia/reoxygenation(H/R) induced damage to cardiomyocytes and the protective effect of hyperoside were examined by means of MTT assay. H/R-induced apoptosis was assessed by Terminal-deoxynucleoitidyl Transferase Mediated Nick End Labeling(TUNEL) and DNA Ladder assay. mRNA expression of Bnip3 was determined by use of quantitative real-time reverse transcription polymerase chain reaction assay. Protein levels of Bnip3, Bax, Bcl-2 and cleaved caspase-3 were examined using western-blot assay. Our results showed that H/R caused great damage to cardiomyocytes, upregulated the protein expressions of Bnip3, Bax, cleaved caspase3, and decreased the expression of the anti-apoptotic protein of Bcl-2. Whereas, compared with the H/R group, a decrease in activities of Bnip3, Bax, cleaved caspase3, and a promoting expression of Bcl-2 were detected in the H/R goup pretreated with hyperoside.
It was concluded in our study that H/R-induced apoptotic effect in cardiomyocytes could be attenuated by hyperoside, and the protective role of hyperoside, if not completely, could be partly through the suppression of the pro-apoptotic gene Bnip3.
•H/R-induced apoptotic effect in cardiomyocytes.•Hyperoside has a protective role in cardiomyocyte apoptosis.•Hyperoside suppress the expression of Bnip3.</abstract><cop>Netherlands</cop><pub>Elsevier B.V</pub><pmid>28754633</pmid><doi>10.1016/j.gene.2017.07.063</doi><tpages>6</tpages></addata></record> |
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| subjects | Animals Apoptosis Bnip3 Cardiotonic Agents - pharmacology Hyperoside Hypoxia/reoxygenation Membrane Proteins - genetics Membrane Proteins - metabolism Mitochondrial Proteins - genetics Mitochondrial Proteins - metabolism Myocardial Infarction - metabolism Myocardial Infarction - pathology Myocytes, Cardiac - drug effects Myocytes, Cardiac - metabolism Myocytes, Cardiac - pathology Plants, Medicinal - chemistry Quercetin - analogs & derivatives Quercetin - pharmacology Rats Rats, Sprague-Dawley Reperfusion Injury - metabolism Reperfusion Injury - pathology |
| title | Hyperoside protects against hypoxia/reoxygenation induced injury in cardiomyocytes by suppressing the Bnip3 expression |
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