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• W4210362535 abstract "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.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.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.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." @default.
• W4210362535 created "2022-02-08" @default.
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• W4210362535 date "2022-01-31" @default.
• W4210362535 modified "2023-10-14" @default.
• W4210362535 title "Putative effect of melatonin on cardiomyocyte senescence in mice with type 1 diabetes mellitus" @default.
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• W4210362535 doi "https://doi.org/10.1007/s40200-022-00982-9" @default.
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