{"title":"Mechanism study of glucose transport by recombinant human brain natriuretic peptide pretreating myocardial cells in rats with hypoxia/reoxygenation","authors":"Lili Tan","doi":"10.3760/CMA.J.ISSN.1673-8799.2017.06.027","DOIUrl":null,"url":null,"abstract":"Objective \nTo investigate the mechanism of glucose transport by recombinant human brain natriuretic peptide(rh-BNP) pretreating myocardial cells in rats with hypoxia/reoxygenation. \n \n \nMethods \nLeft ventricular cardiomyocytes were obtained from SD rats aged 6~8 weeks and were cultured in vitro.They were divided randomly into 5 groups including the control group, hypoxia group, hypoxia/reoxygenation group, rh-BNP pretreating hypoxia group and rh-BNP pretreating hypoxia/reoxygenation group.MTT assay was used to detect the changes of cells viability.The levels of lactate dehydrogenase(LDH), glutathione, superoxide dismutase(SOD) and BNP were measured by ELISA.The expression of iNOS, eNOS, GLUT1 and GLUT4 were detected by RT-PCR. \n \n \nResults \nThe rh-BNP intervention significantly increased the viability of hypoxia and hypoxia/reoxygenation treated cardiomyocytes(P<0.05), reduced the levels of LDH, glutathione, SOD and BNP induced by hypoxia and hypoxia/reoxygenation(P<0.05), and increased the mRNA expression of iNOS, eNOS, GLUT1 and GLUT4 in cardiomyocytes(P<0.05). \n \n \nConclusion \nThe rh-BNP alleviates hypoxia/reoxygenation-induced cardiomyocytes injury by affecting oxidative stress and the expression of GLUT1 and GLUT4. \n \n \nKey words: \nRecombinant human brain natriuretic peptide; Hypoxia/Reoxygenation; Glucose transporter; Oxidative stress","PeriodicalId":64135,"journal":{"name":"中国临床实用医学","volume":"8 1","pages":"92-96"},"PeriodicalIF":0.0000,"publicationDate":"2017-12-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"中国临床实用医学","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.3760/CMA.J.ISSN.1673-8799.2017.06.027","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
Objective
To investigate the mechanism of glucose transport by recombinant human brain natriuretic peptide(rh-BNP) pretreating myocardial cells in rats with hypoxia/reoxygenation.
Methods
Left ventricular cardiomyocytes were obtained from SD rats aged 6~8 weeks and were cultured in vitro.They were divided randomly into 5 groups including the control group, hypoxia group, hypoxia/reoxygenation group, rh-BNP pretreating hypoxia group and rh-BNP pretreating hypoxia/reoxygenation group.MTT assay was used to detect the changes of cells viability.The levels of lactate dehydrogenase(LDH), glutathione, superoxide dismutase(SOD) and BNP were measured by ELISA.The expression of iNOS, eNOS, GLUT1 and GLUT4 were detected by RT-PCR.
Results
The rh-BNP intervention significantly increased the viability of hypoxia and hypoxia/reoxygenation treated cardiomyocytes(P<0.05), reduced the levels of LDH, glutathione, SOD and BNP induced by hypoxia and hypoxia/reoxygenation(P<0.05), and increased the mRNA expression of iNOS, eNOS, GLUT1 and GLUT4 in cardiomyocytes(P<0.05).
Conclusion
The rh-BNP alleviates hypoxia/reoxygenation-induced cardiomyocytes injury by affecting oxidative stress and the expression of GLUT1 and GLUT4.
Key words:
Recombinant human brain natriuretic peptide; Hypoxia/Reoxygenation; Glucose transporter; Oxidative stress
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