2017Zhongguo linchuang shiyong yixueRequires access

Mechanism study of glucose transport by recombinant human brain natriuretic peptide pretreating myocardial cells in rats with hypoxia/reoxygenation

Lili Tan

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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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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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Available 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

Key concepts: GLUT1, Hypoxia (environmental), Brain natriuretic peptide, GLUT4, Glucose transporter, Lactate dehydrogenase, Internal medicine, Oxidative stress

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