Galectin-3 mediates high-glucose-induced cardiomyocyte injury by NADPH oxidase/reactive oxygen species pathway.

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 (STZ)-induced DCM led to high blood glucose level, oxidative stress, cardiac injury, and dysfunction, accompanied by suppressed body weight. On the contrary, MCP (100 mg/kg/day) administration improved body weight 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 malonydialdehyde, although it did not change superoxide dismutase (SOD) 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 (NOX) 4, were obviously increased in the DCM group, while it was 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. PMID: 32311288 [PubMed - as supplied by publisher]
Source: Canadian Journal of Physiology and Pharmacology - Category: Drugs & Pharmacology Authors: Tags: Can J Physiol Pharmacol Source Type: research