The aim of this study was to observe whether necroptosis is involved in the process of
cardiac hypertrophy induced by pressure overload. SD rats underwent transverse abdominal aortic constriction (TAC) operation for establishing
cardiac hypertrophy model. The structure and function of the left ventricle of rats were evaluated via echocardiography, left ventricular mass index, the expression of markers of
cardiac hypertrophy and histological detection. Real-time PCR and Western blot were used to measure the gene and
protein expression of receptor interacting
protein kinase 1 and 3 (RIPK1 and RIPK3, the necroptosis markers) respectively. Four weeks after TAC operation, rat model for
cardiac hypertrophy was established. The experimental data showed that the gene and
protein expressions of RIPK1 and RIPK3 in the rat heart hypertrophic tissues after TAC for 4 weeks were increased significantly compared with those in the
sham group. HE staining showed cardiomyocytes injury and
hypertrophy in the hearts of TAC rat models. By transmission electron microscope, we observed that mitochondria of cardiomyocytes were damaged seriously in the TAC models. Treatment with
losartan used, the selective antagonist of
angiotensin II type I receptor could improve the cardiac function of TAC rats. Moreover,
losartan treatment decreased the expression of RIPK1 and RIPK3 in heart tissues of TAC rats. The results suggest that necroptosis occurrs in the process of
cardiac hypertrophy with pressure overload, and
losartan could alleviate the
cardiac hypertrophy and inhibit necroptosis.