Abstract

The caspase-3-cleaved presence was evaluated in this study in the heart of irradiated rats, during the decline of ventricular function. Female Wistar rats were irradiated with a single dose of radiation (15 Gy) delivered directly to the heart and the molecular, histological and physiological evaluations were performed at thirteen months post-irradiation. The expressions of procollagen type I, TGF-ß1 and caspase-3-cleaved were analyzed using Western blotting. Cardiac structural and functional alterations were investigated by echocardiography and electron microscopy. In the irradiated group, the levels of procollagen type I, TGF-ß1 and caspase-3-cleaved are increased. Significant histological changes (degeneration of heart tissue and collagen deposition) and functional (reduced ejection fraction) were observed. Data suggest that the cardiac function decline after exposure to ionizing radiation is related, in part, to increased collagen and increased caspase-3-cleaved.

Highlights

  • Technological advancement in treatment of cancer combined with early detection and diagnosis have improved the survival of patients suffering fromSAMARA C

  • Increased interstitial fibrosis is an important event in the radiation induced heart disease (RIHD) (Darby et al 2010, Boerma and HauerJensen 2010)

  • This has been observed in patients exposed to radiation in the thoracic region and in heart irradiated animal studies

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Summary

Introduction

Technological advancement in treatment of cancer combined with early detection and diagnosis have improved the survival of patients suffering fromSAMARA C. Technological advancement in treatment of cancer combined with early detection and diagnosis have improved the survival of patients suffering from. In clinical treatments part of the heart may be irradiated (Baker et al 2009). Among other problems a diffuse myocardial fibrosis can be observed. It consists of diffuse proliferation of separating bands of collagen and/or replacing myocytes (Darby et al 2010). Experimental studies show that this condition results in damage to the myocardial capillaries endothelium, causing a decrease in capillary density and can lead to fibrosis (Fajardo and Stewart 1973). Myocardial fibrosis may lead to congestive heart failure (Darby et al 2010). An imbalance between vascular homeostasis and repair pathways, mediated in part by aberrant signaling by TGF-β1, has been implicated in this process (Stewart et al 2010)

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