Abstract
ObjectiveThis study aimed to investigate the protective role of the signal transducer and activator of transcription 4 (STAT4) in diabetic cardiomyopathy. Materials and methodsMale Sprague-Dawley (SD) rats (6–8 weeks old) were purchased from the Experimental Animal Center of Zhengzhou University. The rats were randomly divided into the control and diabetic cardiomyopathy groups. Rat models of diabetic cardiomyopathy were established by a high-sugar and high-fat diet combined with a peritoneal injection of streptozocin. Pathological changes in the heart were visualized using Hematoxylin-eosin (HE) staining and Masson’s staining. Moreover, cell apoptosis was detected using terminal deoxyribonucleotidyl transferase (TdT)-mediated biotin-16-dUTP nick-end labeling (TUNEL) staining and Annexin V apoptosis detection kit. Furthermore, H9C2 cells were transfected with lentivirus overexpressing STAT4 and treated with high glucose. The CCK-8 assay was performed to determine cell viability. Finally, Western blotting was used to determine the expression of STAT4, Bax, and Bcl-2. ResultsThe myocardial tissue of the diabetic cardiomyopathy models showed hypertrophy, myocardial fibrosis and collagen deposition. Furthermore, TUNEL staining showed increased apoptosis and decreased expression of STAT4 in the myocardial cells. Moreover, the myocardial tissues of the DCM models showed increased expression of Bax/Bcl-2 and a high percentage of Annexin V positive cells. The H9C2 cells showed decreased expression of STAT4 following high glucose treatment. However, the H9C2 cells overexpressing STAT4 showed decreased expression of Bax/Bcl-2 and reduced percentage of Annexin V positive cells. ConclusionThe DCM group had decreased myocardial expression of STAT4. Furthermore, overexpression of STAT4 was shown to reduce high glucose-induced apoptosis.
Published Version
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call