Abstract

The severity of the development of uremic cardiomyopathy (UC) and fibrosis of cardiac tissue at chronic renal failure (CRF) was compared in the model experiments on male Sprague-Dawley and Wistar rats of the SPF category. To induce CRF in rats, subtotal nephrectomy (NE) was performed on the left, and after 2 weeks, total nephrectomy on the right. Sham-operated (Sham) animals served as controls. 4 weeks after the second surgery, blood pressure (BP) was measured in animals, and the expression of fibrotic factors (transcription factor Fli1, pro-collagen-I, collagen-I and collagen-IV) in the tissues of heart left ventricle was evaluated by real-time PCR and immunoblotting. After NE, Sprague-Dawley rats exhibited a significant increase in systolic blood pressure and left ventricular hypertrophy. In Wistar rats, the difference in BP between NE and Sham animals was smaller, and the ratio of left ventricular mass to body weight did not change. Experimental CRF in Sprague-Dawley rats was accompanied by a 1.5–2.5-fold suppression of the Fli1 gene expression and a decrease in the content of Fli1 protein in the cardiac tissue, while no significant differences were observed in Wistar rats. The levels of pro-collagen-I and collagen-I in the heart of rats of both lines did not change either at the levels of transcription or translation. Such difference in development of pathological processes indicates ineffectiveness of applied NE scheme for induction of UC and investigation of pro-fibrotic processes in Wistar rats.

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