Isosteviol ameliorates diabetic cardiomyopathy in rats by inhibiting ERK and NF-κB signaling pathways

Tang, S, Liu, X, Ye, J, Hu, T, Yang, Y, Han, T and Tan, W 2018, 'Isosteviol ameliorates diabetic cardiomyopathy in rats by inhibiting ERK and NF-κB signaling pathways', Journal of Endocrinology, vol. 238, no. 1, pp. 47-60.

Document type: Journal Article
Collection: Journal Articles

Title Isosteviol ameliorates diabetic cardiomyopathy in rats by inhibiting ERK and NF-κB signaling pathways
Author(s) Tang, S
Liu, X
Ye, J
Hu, T
Yang, Y
Han, T
Tan, W
Year 2018
Journal name Journal of Endocrinology
Volume number 238
Issue number 1
Start page 47
End page 60
Total pages 14
Publisher BioScientifica
Abstract Diabetes-induced injury of myocardium, defined as diabetic cardiomyopathy (DCM), accounts for significant mortality and morbidity in diabetic population. Alleviation of DCM by a potent drug remains considerable interests in experimental and clinical researches because hypoglycemic drugs cannot effectively control this condition. Here, we explored the beneficial effects of isosteviol sodium (STVNa) on type 1 diabetesinduced DCM and the potential mechanisms involved. Male Wistar rats were induced to diabetes by injection of streptozotocin (STZ). One week later, diabetic rats were randomly grouped to receive STVNa (STZ/STVNa) or its vehicle (STZ). After 11 weeks of treatment or 11 weeks treatment following 4 weeks of removal of the treatment, the cardiac function and structure were evaluated and related mechanisms were investigated. In diabetic rats, oxidative stress, inflammation, blood glucose and plasma advanced glycation end products (AGEs) were significantly increased, whereas superoxide dismutase 2 (SOD-2) expression and activity were decreased. STVNa treatment inhibited cardiac hypertrophy, fibrosis and inflammation, showed similar ratio of heart to body weight and antioxidant capacities almost similar to the normal controls, which can be sustained at least 4 weeks. Moreover, STVNa inhibited diabetesinducted stimulation of both extracellular signal-regulated kinase (ERK) and nuclear factor κB (NF-κB) signal pathways. However, blood glucose, plasma AGE and insulin levels were not altered by STVNa treatment. These results indicate that STVNa may be developed into a potent therapy for DCM. The mechanism underlying this therapeutic effect involves the suppression of oxidative stress and inflammation by inhibiting ERK and NF-κB without changing blood glucose or AGEs.
Subject Endocrinology
Keyword(s) Advanced glycation end products
Diabetic cardiomyopathy
Extracellular signalregulated kinase
Oxidative stress
DOI - identifier 10.1530/JOE-17-0681
Copyright notice © 2018 Society for Endocrinology
ISSN 0022-0795
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