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The protective effects of S14G-humanin (HNG) against streptozotocin (STZ)-induced cardiac dysfunction
Xiaopan Chen1, Chuan Yun1, Hailong Zheng1
1Department Of Endocrinology, The First Affiliated Hospital of Hainan Medical University, Hainan, China.
Insights
S14G-humanin (HNG) protects against diabetic cardiomyopathy by reducing myocardial hypertrophy and improving heart function. This peptide inhibits the p38/NF-κB pathway, offering a potential therapeutic strategy for diabetic heart disease.
Area of Science:
- Cardiology
- Endocrinology
- Molecular Biology
Background:
- Diabetic cardiomyopathy (DCM) is characterized by oxidative stress, inflammation, and myocardial hypertrophy.
- S14G-humanin (HNG), a humanin analogue, exhibits cytoprotective properties in various tissues.
- The therapeutic potential of HNG in DCM remains unexplored.
Purpose of the Study:
- To investigate the protective effects of S14G-humanin (HNG) against streptozotocin (STZ)-induced cardiac dysfunction in a mouse model of diabetes.
- To elucidate the underlying molecular mechanisms of HNG's action in DCM.
Main Methods:
- Streptozotocin (STZ) was administered to induce diabetes and cardiac dysfunction in mice.
- HNG treatment was administered to assess its protective effects.
- Myocardial hypertrophy was evaluated using Wheat Germ Agglutinin (WGA) staining.
- Cardiac function was assessed via echocardiography.
- Biomarkers of myocardial injury (CK-MB, AST, LDH) and inflammatory cytokines (TNF-α, IL-6) were measured.
- Western blotting was used to determine the expression of phosphorylated p38 and p38 MAPK, and NF-κB signaling pathway activation.
Main Results:
- HNG treatment significantly attenuated STZ-induced myocardial hypertrophy and improved cardiac function.
- HNG administration reduced levels of myocardial injury markers (CK-MB, AST, LDH) and inflammatory cytokines (TNF-α, IL-6).
- HNG suppressed the activation of the p38/NF-κB signaling pathway.
Conclusions:
- S14G-humanin (HNG) demonstrates significant protective effects against streptozotocin-induced diabetic cardiomyopathy.
- HNG ameliorates cardiac dysfunction and myocardial injury by inhibiting the p38/NF-κB signaling pathway.
- HNG represents a promising therapeutic candidate for managing diabetic cardiomyopathy.
Abstract:
Excessive oxidative stress, inflammation, and myocardial hypertrophy have been associated with diabetic cardiomyopathy (DCM). S14G-humanin (HNG) is a potent humanin analogue that has demonstrated cytoprotective effects in a variety of cells and tissues. However, the pharmacological function of HNG in diabetic cardiomyopathy has not yet been reported. In the present study, we investigated the protective effects of HNG against streptozotocin (STZ)-induced cardiac dysfunction in diabetic mice. Myocardial hypertrophy in diabetic mice was determined using Wheat Gem Agglutinin (WGA) staining. The heart function was measured with Echocardiographic imaging. Levels of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) proteins in plasma were measured using enzyme-linked immunosorbent assay (ELISA) kits. Protein expression of Phosphorylated p38/p38 was determined using western blots. We found that HNG treatment attenuated the STZ-induced myocardial hypertrophy and significantly improved heart function. Also, its treatment proved effective as it reduced the levels of several myocardial injury indicators, including creatine kinase-MB (CK-MB), aspartate aminotransferase (AST), lactate dehydrogenase (LDH), and both the cardiac and plasma levels of TNF-α and IL-6, highlighting its effect on the STZ-induced myocardial injury. Lastly, HNG suppressed the activation of the p38/nuclear factor kappa-B (NF-κB) signaling pathway. S14G humanin possesses protective effects against streptozotocin-induced cardiac dysfunction through inhibiting the activation of the p38/NF-κB signaling pathway.
