In:
European Journal of Heart Failure, Wiley, Vol. 12, No. 10 ( 2010-10), p. 1051-1060
Abstract:
To evaluate the protective effect of thalidomide, a potent anti‐inflammatory drug, on the development of diabetic cardiomyopathy (DMCMP). Methods and results We 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/μl, 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‐α 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‐α, IL‐1β, ICAM‐1, and VCAM‐1. Conclusion In an animal model of DMCMP, deterioration of LV systolic and diastolic function was partially prevented by thalidomide treatment.
Type of Medium:
Online Resource
ISSN:
1388-9842
,
1879-0844
DOI:
10.1093/eurjhf/hfq103
Language:
English
Publisher:
Wiley
Publication Date:
2010
detail.hit.zdb_id:
1500332-2
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