Putative effect of melatonin on cardiomyocyte senescence in mice with type 1 diabetes mellitus.

Background: To date, many investigators have tried to clarify the molecular mechanism of cardiovascular injuries after T1D. In present study, we evaluated the possible effects of melatonin on the levels of aging-related factors in the heart tissue of streptozotocin-induced diabetic mice.
Methods: 40 male mice were enrolled in this study and randomly allocated into 4 groups (n = 10) as follows: Control group (C), Control group + melatonin (CM), Diabetic group (D), Diabetic + melatonin (DM) group. Single Streptozotocin (50 mg/kbW) was applied for the induction of T1D. 3 mg/kg melatonin was injected intraperitoneally twice a week for consequent four weeks. After the completion of this period, the animals were sacrificed and their heart tissue was obtained for histological examination (IHC analysis of vWF and α-SMA cells), aging and inflammation-related gene analysis. Result: Hematoxylin and Eosin staining indicated cardiomyocyte toxicity in T1D mice. IHC analysis of vascular tissue showed the detachment of vWF and α-SMA cells and disintegration into the vascular lumen. Additionally, real-time PCR assay showed the up-regulation of β-galactosidase and suppression of SOX2, Klotho, and Telomerase genes in T1D mice compared to the control group (p < 0.05). We noted that melatonin administration can revert these condition and closed near-to-control levels. Along with these conditions, the levels of IL-1β were also decreased after melatonin treatment. Conclusions: In general, one can hypothesize that modulation of different effectors associated with aging is beneficial to alleviate cardiac injuries under hypergylcemic condition. Melatonin can exert its therapeutic effects, in part, through anti-aging capacity. © Springer Nature Switzerland AG 2022.