Therapeutic inhibition of galectin-3 improves cardiomyocyte apoptosis and survival during heart failure

Galectin-3 is an important mediator of cardiac fibrosis and heart failure. Cell viability of cardiomyocytes was measured using a CCK-8 assay; flow cytometry was employed for the detection of the cell cycle and cardiomyocytes apoptosis. Reverse transcription-quantitative polymerase chain reaction and western blotting was performed to examine the expression of associated genes and proteins. The present study demonstrated that overexpression of galectin-3 significantly decreased the viability of cardiomyocytes in a time-dependent manner, with simultaneous arrest of the cell cycle and induction of apoptosis. The expression levels of proliferating cell nuclear antigen (PCNA) and B-cell lymphoma 2 (Bcl-2) were decreased and Bcl-2-associated X protein (Bax) was increased in cardiomyocytes with galectin-3 overexpression. However, inhibition of galectin-3 by intravenous tail vein injection of a galectin-3-targeting short hairpin RNA-expressing vector during hypertension-induced heart failure in Dahl hypertensive rats increased rat survival and body weight. Inhibition of galectin-3 also increased the expression of PCNA and Bcl-2 and reduced the expression of Bax in the cardiac tissue of hypertensive rats. These results demonstrate the therapeutic potential of targetinggalectin-3 for the treatment of cardiac disease.