The protective effect of thalidomide on left ventricular function in a rat model of diabetic cardiomyopathy

Dae Hee Kim, Yong Jin Kim, Sung A. Chang, Hye Won Lee, Ha Na Kim, Hyung Kwan Kim, Hyuk-Jae Chang, Dae Won Sohn, Young Bae Park

Research output: Contribution to journalArticle

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Abstract

AimsTo evaluate the protective effect of thalidomide, a potent anti-inflammatory drug, on the development of diabetic cardiomyopathy (DMCMP).Methods and resultsWe induced type 1 diabetes using streptozocin in 8-week-old Sprague-Dawley rats, divided them into two groups-a thalidomide treatment group (DM-T, n = 15) and a non-treatment group (DM-N, n = 15)-and compared them with a normal control (n = 10). Ten weeks after diabetes induction, heart and lung mass indices were higher in the DM-N group compared with the control group. In the DM-T group, increases in heart and lung mass indices were attenuated compared with the DM-N group. On echocardiographic examination, systolic and diastolic mitral annulus velocities were impaired in the DM-N group, but they remained normal in the DM-T group. On haemodynamic analyses, left ventricular (LV) systolic function, represented by end-systolic elastance (0.35 ± 0.14 vs. 0.18 ± 0.07 mmHg/l, P < 0.001) and preload-recruitable stroke work (90.5 ± 24.3 vs. 51.8 ± 22.0 mmHg, P < 0.001), was preserved in the DM-T group compared with the DM-N group. Likewise, deterioration of LV diastolic function was attenuated in the DM-T group. Increases in serum levels of TNF-were attenuated in the DM-T group compared with the DM-N group. On histological analysis, thalidomide treatment lowered total myocardial collagen content and the expression of TNF-, IL-1, ICAM-1, and VCAM-1.ConclusionIn an animal model of DMCMP, deterioration of LV systolic and diastolic function was partially prevented by thalidomide treatment.

Original languageEnglish
Pages (from-to)1051-1060
Number of pages10
JournalEuropean Journal of Heart Failure
Volume12
Issue number10
DOIs
Publication statusPublished - 2010 Oct 1

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Diabetic Cardiomyopathies
Thalidomide
Left Ventricular Function
Lung
Vascular Cell Adhesion Molecule-1
Intercellular Adhesion Molecule-1
Streptozocin
Type 1 Diabetes Mellitus
Interleukin-1
Sprague Dawley Rats
Anti-Inflammatory Agents
Collagen
Animal Models
Hemodynamics
Stroke
Control Groups
Serum
Pharmaceutical Preparations

All Science Journal Classification (ASJC) codes

  • Cardiology and Cardiovascular Medicine

Cite this

Kim, D. H., Kim, Y. J., Chang, S. A., Lee, H. W., Kim, H. N., Kim, H. K., ... Park, Y. B. (2010). The protective effect of thalidomide on left ventricular function in a rat model of diabetic cardiomyopathy. European Journal of Heart Failure, 12(10), 1051-1060. https://doi.org/10.1093/eurjhf/hfq103
Kim, Dae Hee ; Kim, Yong Jin ; Chang, Sung A. ; Lee, Hye Won ; Kim, Ha Na ; Kim, Hyung Kwan ; Chang, Hyuk-Jae ; Sohn, Dae Won ; Park, Young Bae. / The protective effect of thalidomide on left ventricular function in a rat model of diabetic cardiomyopathy. In: European Journal of Heart Failure. 2010 ; Vol. 12, No. 10. pp. 1051-1060.
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The protective effect of thalidomide on left ventricular function in a rat model of diabetic cardiomyopathy. / Kim, Dae Hee; Kim, Yong Jin; Chang, Sung A.; Lee, Hye Won; Kim, Ha Na; Kim, Hyung Kwan; Chang, Hyuk-Jae; Sohn, Dae Won; Park, Young Bae.

In: European Journal of Heart Failure, Vol. 12, No. 10, 01.10.2010, p. 1051-1060.

Research output: Contribution to journalArticle

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T1 - The protective effect of thalidomide on left ventricular function in a rat model of diabetic cardiomyopathy

AU - Kim, Dae Hee

AU - Kim, Yong Jin

AU - Chang, Sung A.

AU - Lee, Hye Won

AU - Kim, Ha Na

AU - Kim, Hyung Kwan

AU - Chang, Hyuk-Jae

AU - Sohn, Dae Won

AU - Park, Young Bae

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N2 - AimsTo evaluate the protective effect of thalidomide, a potent anti-inflammatory drug, on the development of diabetic cardiomyopathy (DMCMP).Methods and resultsWe induced type 1 diabetes using streptozocin in 8-week-old Sprague-Dawley rats, divided them into two groups-a thalidomide treatment group (DM-T, n = 15) and a non-treatment group (DM-N, n = 15)-and compared them with a normal control (n = 10). Ten weeks after diabetes induction, heart and lung mass indices were higher in the DM-N group compared with the control group. In the DM-T group, increases in heart and lung mass indices were attenuated compared with the DM-N group. On echocardiographic examination, systolic and diastolic mitral annulus velocities were impaired in the DM-N group, but they remained normal in the DM-T group. On haemodynamic analyses, left ventricular (LV) systolic function, represented by end-systolic elastance (0.35 ± 0.14 vs. 0.18 ± 0.07 mmHg/l, P < 0.001) and preload-recruitable stroke work (90.5 ± 24.3 vs. 51.8 ± 22.0 mmHg, P < 0.001), was preserved in the DM-T group compared with the DM-N group. Likewise, deterioration of LV diastolic function was attenuated in the DM-T group. Increases in serum levels of TNF-were attenuated in the DM-T group compared with the DM-N group. On histological analysis, thalidomide treatment lowered total myocardial collagen content and the expression of TNF-, IL-1, ICAM-1, and VCAM-1.ConclusionIn an animal model of DMCMP, deterioration of LV systolic and diastolic function was partially prevented by thalidomide treatment.

AB - AimsTo evaluate the protective effect of thalidomide, a potent anti-inflammatory drug, on the development of diabetic cardiomyopathy (DMCMP).Methods and resultsWe induced type 1 diabetes using streptozocin in 8-week-old Sprague-Dawley rats, divided them into two groups-a thalidomide treatment group (DM-T, n = 15) and a non-treatment group (DM-N, n = 15)-and compared them with a normal control (n = 10). Ten weeks after diabetes induction, heart and lung mass indices were higher in the DM-N group compared with the control group. In the DM-T group, increases in heart and lung mass indices were attenuated compared with the DM-N group. On echocardiographic examination, systolic and diastolic mitral annulus velocities were impaired in the DM-N group, but they remained normal in the DM-T group. On haemodynamic analyses, left ventricular (LV) systolic function, represented by end-systolic elastance (0.35 ± 0.14 vs. 0.18 ± 0.07 mmHg/l, P < 0.001) and preload-recruitable stroke work (90.5 ± 24.3 vs. 51.8 ± 22.0 mmHg, P < 0.001), was preserved in the DM-T group compared with the DM-N group. Likewise, deterioration of LV diastolic function was attenuated in the DM-T group. Increases in serum levels of TNF-were attenuated in the DM-T group compared with the DM-N group. On histological analysis, thalidomide treatment lowered total myocardial collagen content and the expression of TNF-, IL-1, ICAM-1, and VCAM-1.ConclusionIn an animal model of DMCMP, deterioration of LV systolic and diastolic function was partially prevented by thalidomide treatment.

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