IL-35 Ameliorates Myocardial Strain in Mice with T2DM-Induced Cardiac Injury: Assessment by Layer-Specific Strain

The established association between endothelial dysfunction and the pathogenesis of cardiovascular disease in diabetic individuals has been well-documented. Interleukin-35 (IL-35) can suppress inflammatory processes and ameliorate endothelial dysfunction. This study aimed to evaluate the effect of IL-35 treatment on diabetic mice with diabetes-induced cardiac injury using layer-specific strain analysis.

Twenty-six mice were allocated into three groups: the control group (CON, n=10), the diabetic group (DM, n=10), and the diabetic group treated with IL-35 (DMIL, n=6). The DM and DMIL groups were subjected to a high-fat diet and streptozotocin to induce diabetes, with the DMIL group receiving an additional 6 weeks of IL-35 treatment. Measurements of body weight, blood glucose levels, routine echocardiographic parameters, and layer-specific strain were conducted at baseline, post-diabetes induction, and post-treatment. Morphological changes in cardiomyocytes were examined in pathological heart sections, and cardiac inflammation was detected by protein immunoblotting.

After inducing diabetes, diabetic mice exhibited notable systolic and diastolic dysfunction. IL-35 treatment significantly reduced myocardial inflammatory infiltration and improved myocardial fibrosis in the DMIL group in comparison to the DM group. Only diastolic function E/e' showed a significant improvement when comparing conventional echocardiograms between the DMIL and DM groups. In the context of layered strain analysis, the DMIL group exhibited a notable enhancement in middle and epicardial global longitudinal strain and global radial strain when compared to the DM group.

IL-35 can enhance myocardial function in diabetic mice. Layer-specific strain could serve as a valuable tool for evaluating interventions in diabetes.