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A Simple and Efficient Method for In Vivo Cardiac-specific Gene Manipulation by Intramyocardial Injection in Mice
Published on: April 16, 2018
Putative effect of melatonin on cardiomyocyte senescence in mice with type 1 diabetes mellitus
Reza Rahbarghazi1,2, Mohammad Farhoudi3,4, Hamed Rahmani-Youshanlouei3,4
1Stem Cell Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
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.
Insights
Melatonin treatment improved cardiac health in diabetic mice by reducing aging factors and inflammation. This suggests melatonin
Area of Science:
- Cardiovascular Research
- Endocrinology
- Gerontology
Background:
- Cardiovascular complications are a significant concern in Type 1 Diabetes (T1D).
- The molecular mechanisms underlying T1D-induced cardiac injury are not fully understood.
- Aging-related factors may play a role in the development of diabetic cardiomyopathy.
Purpose of the Study:
- To investigate the effects of melatonin on aging-related factors in the heart tissue of diabetic mice.
- To evaluate the potential therapeutic role of melatonin in mitigating cardiac damage associated with Type 1 Diabetes.
Main Methods:
- Male mice were induced with Type 1 Diabetes using streptozotocin.
- Mice were treated with melatonin (3 mg/kg) or vehicle for four weeks.
- Heart tissues were analyzed for cardiomyocyte toxicity, vascular integrity (vWF, α-SMA), and expression of aging/inflammation genes (β-galactosidase, SOX2, Klotho, Telomerase, IL-1β).
Main Results:
- Diabetic mice exhibited cardiomyocyte toxicity and vascular damage.
- Type 1 Diabetes led to increased β-galactosidase and decreased SOX2, Klotho, and Telomerase gene expression.
- Melatonin treatment reversed these changes, restoring near-control levels and reducing IL-1β.
Conclusions:
- Modulating aging-related factors is beneficial for alleviating cardiac injury in hyperglycemia.
- Melatonin demonstrates therapeutic potential in treating diabetic cardiac complications.
- Melatonin's anti-aging properties contribute to its protective effects against diabetic heart disease.
