Journal
CANADIAN JOURNAL OF PHYSIOLOGY AND PHARMACOLOGY
Volume 94, Issue 3, Pages 332-340Publisher
CANADIAN SCIENCE PUBLISHING
DOI: 10.1139/cjpp-2015-0073
Keywords
advanced glycation end products; diabetic cardiomyopathy; inflammatory cytokines; NF-kappa B; mangiferin
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Funding
- State Administration of Traditional Chinese Medicine of the General Logistics Department [10ZYZ120]
- National Natural Science Foundation of China [81170216]
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Given the importance of the aggregation of advanced glycation end products (AGEs) and cardiac inflammation in the onset and progression of diabetic cardiomyopathy (DCM), our objective in this study was to demonstrate the cardioprotective effect of mangiferin, an antidiabetic and anti-inflammatory agent, on diabetic rat model. The DCM model was established by a high-fat diet and a low dose of streptozotocin. DCM rats were treated orally with mangiferin (20 mg/kg) for 16 weeks. Serum and left ventricular myocardium were collected for determination of inflammatory cytokines. AGEs mRNA and protein expression of nuclear factor kappa B (NF-kappa B) and receptor for AGEs (RAGE) in myocardium were assayed by real-time PCR and Western blot. ROS levels were measured by dihydroethidium fluorescence staining. NF-kappa B binding activity was assayed by TransAM NF-kappa B p65 ELISA kit. Chronic treatment with mangiferin decreased the levels of myocardial enzymes (CK-MB, LDH) and inflammatory mediators (TNF-alpha, IL-1 beta). Meanwhile, NF-kappa B is inhibited by the reduction of nuclear translocation of p65 subunit, and mangiferin reduced AGE production and decreased the mRNA and protein expression of RAGE in DCM rats. Our data indicated that mangiferin could significantly ameliorate DCM by preventing the release of inflammatory cytokines, and inhibiting ROS accumulation, AGE/RAGE production, and NF-kappa B nuclear translocation, suggesting that mangiferin treatment might be beneficial in DCM.
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