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- Title
Galectin-3 mediates high-glucose-induced cardiomyocyte injury by the NADPH oxidase/reactive oxygen species pathway.
- Authors
Sun, Jingang; Zhang, Lijuan; Fang, Jianhai; Yang, Shuguo; Chen, Lianghua
- Abstract
Galectin-3 is a member of the β-galactoside-binding lectin family taking part in the regulation of inflammation, angiogenesis, and fibrosis. This study was designed to study the improved effect of galectin-3 inhibition on diabetic cardiomyopathy (DCM). Sprague–Dawley rats were randomized into the control, DCM, and DCM + modified citrus pectin (MCP) (a galectin–3 pharmacological inhibitor) groups. After 8 weeks, streptozotocin-induced DCM led to high blood glucose level, oxidative stress, cardiac injury, and dysfunction accompanied by suppressed body mass. On the contrary, MCP (100 mg·kg−1·day−1) administration improved body mass and blood glucose level and attenuated cardiac injury and dysfunction in DCM rats. Additionally, MCP attenuated pathological changes in plasma and myocardial tissue markers of oxidative stress, such as hydrogen peroxide and malonyldialdehyde, although it did not change superoxide dismutase activities, which were decreased in the DCM group. The levels of oxidative stress associated proteins evaluated by Western blot, such as p67phox and NADPH oxidase 4, were obviously increased in the DCM group, while they were reversed by MCP treatment. Therefore, galectin-3-mediated high-glucose-induced cardiomyocyte injury and galectin-3 inhibition attenuated DCM by suppressing NADPH oxidase. These findings suggested that galectin-3 could be a potential target for treatment of patients with DCM.
- Subjects
REACTIVE oxygen species; NADPH oxidase; GALECTINS; HEAT shock proteins; STREPTOZOTOCIN; HEART diseases
- Publication
Canadian Journal of Physiology & Pharmacology, 2020, Vol 98, Issue 11, p826
- ISSN
0008-4212
- Publication type
Article
- DOI
10.1139/cjpp-2019-0708