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Galectin-3 Inhibition Ameliorates Streptozotocin-Induced Diabetic Cardiomyopathy in Mice
Ning Zhu1, Liuyan Zhu2, Bingwu Huang3
1Department of Cardiology, The Third Affiliated Hospital of Shanghai University, The Wenzhou Third Clinical Institute Affiliated to Wenzhou Medical University, Wenzhou People's Hospital, Wenzhou, China.
Insights
Galectin-3 (Gal-3) inhibition ameliorates diabetic cardiomyopathy (DCM) by reducing cardiac apoptosis, inflammation, and fibrosis. This study clarifies Gal-3
Area of Science:
- Cardiovascular Biology and Disease
- Metabolic Disorders and Endocrinology
- Molecular and Cellular Pathology
Background:
- Diabetic cardiomyopathy (DCM) is a significant complication of diabetes, increasing heart failure risk.
- The role of Galectin-3 (Gal-3) in DCM pathogenesis, particularly its regulation of cardiac inflammation and fibrosis, requires elucidation.
- Understanding Gal-3's mechanism in DCM is crucial for developing targeted therapies.
Purpose of the Study:
- To investigate whether Gal-3 inhibition can attenuate cardiac dysfunction and pathological changes in a mouse model of DCM.
- To determine the effect of Gal-3 knockdown on myocardial apoptosis, oxidative stress, inflammation, and fibrosis in DCM.
- To elucidate the molecular mechanism involving Gal-3 and NF-κB p65 activation in DCM pathogenesis.
Main Methods:
- Diabetic cardiomyopathy (DCM) was induced in mice using streptozotocin.
- Cardiac function and structure were assessed via echocardiography and histological analysis.
- Myocardial injury, apoptosis, oxidative stress, fibrosis, and inflammatory markers were quantified using ELISA, PCR, TUNEL, and Western blotting.
Main Results:
- Gal-3 knockdown significantly improved cardiac function and reduced myocardial apoptosis, oxidative stress, inflammation, and fibrosis in DCM mice.
- Silencing Gal-3 suppressed high glucose-induced macrophage infiltration and inflammatory cytokine release in vitro.
- A regulatory network involving Gal-3 and NF-κB p65 was identified as critical in DCM development.
Conclusions:
- Galectin-3 inhibition ameliorates DCM by reducing myocardial apoptosis, oxidative stress, inflammation, and fibrosis.
- Gal-3 appears to promote DCM progression, at least partly, by modulating NF-κB p65 activation.
- Targeting Gal-3 represents a potential therapeutic strategy for managing diabetic cardiomyopathy.
Objective:
Diabetic cardiomyopathy (DCM), characterized by cardiomyopathy with the absence of coronary artery disease, hypertension, and valvular heart disease in patients with diabetes, significantly increases the risk of heart failure. Galectin-3 (Gal-3) has been shown to regulate cardiac inflammation and fibrosis, but its role in DCM remains unclear. This study aimed to determine whether Gal-3 inhibition attenuates DCM and NF-κB p65 activation.
Methods:
Diabetic cardiomyopathy (DCM) was established by intraperitoneal (IP) injection of streptozotocin for 5 consecutive days in mice. Myocardial injury markers, such as creatine kinase isoenzyme (CK-BM) and lactate dehydrogenase, were detected using ELISA. We used non-invasive transthoracic echocardiography to examine cardiac structure and function. Histological staining was used to explore myocardial morphology and fibrosis. Profibrotic markers and inflammatory cytokines were detected by ELISA and real-time PCR in vivo. The terminal deoxyribonucleotide transferasemediated dUTP nick end-labeling (TUNEL) and immunofluorescence assays were conducted to examine myocardial apoptosis and oxidative stress. Inflammatory cytokines induced by high glucose (HG) were also found in RAW264.7 macrophages. The underlying molecular mechanisms were determined using immunofluorescence and Western blotting analyses.
Results:
The Gal-3 knockdown was observed to ameliorate myocardial apoptosis, oxidative stress, inflammatory cytokines release, macrophage infiltration, and fibrosis, thus, decreasing cardiac dysfunction in DCM mice. In addition, the silence of Gal-3 could suppress macrophage infiltration and inflammatory cytokine release induced by HG. Finally, a Gal-3/NF-κB p65 regulatory network was clarified in the pathogenesis of DCM.
Conclusion:
The Gal-3 may promote myocardial apoptosis, oxidative stress, inflammation, and fibrosis in vivo and in vitro by the mechanism of reduction of NF-κB p65 activation.
