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Repeated Humanin Treatment Attenuates Oxidative Stress, Inflammation, and Apoptosis in Diabetic Cardiac Tissue
Ferah Bulut1, Muhammed Adam1, Munevver Gizem Hekim2
1Department of Biophysics, Faculty of Medicine, Firat University, Elazig TR23119, Turkey.
Insights
Humanin (HN) peptide treatment protects the heart from diabetes-induced damage by reducing oxidative stress, inflammation, and apoptosis. This suggests HN may be a potential therapy for diabetic cardiovascular complications.
Area of Science:
- Cardiovascular Research
- Metabolic Disorders
- Mitochondrial Biology
Background:
- Diabetes mellitus (DM) significantly elevates cardiovascular disease risk via hyperglycemia-induced oxidative stress, inflammation, and apoptosis.
- Humanin (HN), a cytoprotective peptide, shows antioxidant and anti-apoptotic potential, but its role in diabetic cardiac injury is unclear.
Purpose of the Study:
- To investigate the protective effects of repeated Humanin (HN) treatment against streptozotocin (STZ)-induced cardiac injury in a mouse model.
- To evaluate HN's impact on oxidative stress, inflammation, and apoptosis in diabetic hearts.
Main Methods:
- Mice were divided into control, HN-treated, STZ-induced diabetic, and STZ + HN-treated groups (n=10/group).
- HN (4 mg/kg) was administered daily for 15 days.
- Biochemical analyses assessed oxidative stress, inflammatory cytokines, and apoptotic markers.
Main Results:
- STZ-induced diabetes increased oxidative stress, pro-inflammatory cytokines, and apoptosis while decreasing antioxidant and anti-inflammatory markers.
- Repeated HN treatment significantly attenuated these diabetes-induced changes.
- HN treatment restored redox and inflammatory balance in diabetic cardiac tissue.
Conclusions:
- Repeated Humanin (HN) treatment effectively mitigates oxidative stress, inflammation, and apoptosis in diabetic mouse hearts.
- HN demonstrates potential as a therapeutic agent for managing diabetes-associated cardiac complications.
Abstract:
Diabetes mellitus (DM) markedly increases the risk of cardiovascular complications through mechanisms involving hyperglycemia-induced oxidative stress, inflammation, and apoptosis. Humanin (HN), a mitochondria-derived peptide with established cytoprotective properties, has been reported to exert antioxidant and anti-apoptotic effects in several experimental models. However, its role in diabetic cardiac injury remains insufficiently understood. The present study investigated the protective effects of repeated HN treatment against diabetes-induced cardiac injury in a streptozotocin (STZ)-induced mouse model. Mice were divided into four groups: control, HN-treated, STZ-induced diabetic, and STZ + HN-treated groups (n = 10/group). HN (4 mg/kg) was administered daily for 15 consecutive days. Biochemical analyses were performed to evaluate oxidative stress, inflammatory cytokines, and apoptotic markers. STZ-induced diabetes significantly increased oxidative stress markers, pro-inflammatory cytokines, and apoptotic activity while reducing antioxidant defenses and anti-inflammatory cytokines compared with controls. Repeated HN treatment markedly attenuated these alterations and restored redox and inflammatory balance in diabetic cardiac tissue. These findings demonstrate that repeated HN treatment attenuates oxidative stress, inflammation, and apoptosis in the hearts of diabetic mice. The results further suggest that HN may represent a promising therapeutic candidate for limiting diabetes-associated cardiac complications.

