Mangiferin suppressed advanced glycation end products (AGEs) through NF-κB deactivation and displayed anti-inflammatory effects in streptozotocin and high fat diet-diabetic cardiomyopathy rats
Abstract
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-κB) 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-κB binding activity was assayed by TransAM NF-κB p65 ELISA kit. Chronic treatment with mangiferin decreased the levels of myocardial enzymes (CK-MB, LDH) and inflammatory mediators (TNF-α, IL-1β). Meanwhile, NF-κB 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-κB nuclear translocation, suggesting that mangiferin treatment might be beneficial in DCM.
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In rat models of diabetic cardiomyopathy, MGF (20 mg/kg for 16 weeks) decreases ROS production and AGE accumulation partly through inhibition of NF-κB signaling, preserving myocardial function and delaying cardiomyopathic remodeling.
“In rat models of diabetic cardiomyopathy, MGF (20 mg/kg for 16 weeks) has been shown to notably decrease ROS production and AGE accumulation, partly through the inhibition of NF-κB signaling. This preserves myocardial function and delays cardiomyopathic remodeling (149).”
From Mangiferin in human disease: Multifaceted mechanisms and applications (Review) (2026) · cites this paper as [149]
In diabetic cardiomyopathy rats, mangiferin reduces AGE production and decreases mRNA and protein expression of RAGE.
“In diabetic cardiomyopathy (DCM) rats, mangiferin reduces AGE production, and decreases the mRNA and protein expression of RAGE (42), suggesting that mangiferin treatment may be beneficial in DCM.”
From Mangiferin: An effective therapeutic agent against several disorders (Review) (2018) · cites this paper as [42]
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- Authors
- Hou, J., Zheng, D., Fung, G., Deng, H., Chen, L., Liang, J., Jiang, Y., & Hu, Y.
- Affiliations
- University of British Columbia (CA)
- General Hospital of Jinan Military Command (CN)
- Army Medical University (CN)
- Department of Cardiovascular Surgery, Jinan Military General Hospital, Jinan, China.
- Chengdu Military General Hospital (CN)
- Corresponding author
- Hou, Jun
- Zheng, Dezhi
- Venue
- Canadian Journal of Physiology and Pharmacology
- Publisher
- Canadian Science Publishing
- Published
- 2016-03
- Volume
- 94
- Issue
- 3
- Pages
- 332-340
- ISSN
- 0008-4212 (ISSN-L)
- 1205-7541
- OpenAlex
- W1952394616
- Cited by
- 89
- References
- 34
- Citations by year
- 2026: 4 · 2025: 10 · 2024: 8 · 2023: 8 · 2022: 1 · 2021: 12 · 2020: 11 · 2019: 6 · 2018: 7 · 2017: 16 · 2016: 6
- FWCI
- 18.98
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Canadian Journal of Physiology and Pharmacology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Complementary and alternative medicine › Mangiferin and Mango Extracts
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Advanced Glycation End Products research
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Natural Antidiabetic Agents Studies
- Keywords
- mangiferin, advanced glycation end products, diabetic cardiomyopathy, NF-κB, receptor for advanced glycation end products, cardiac inflammation, oxidative stress, streptozotocin-induced diabetes, high-fat diet, anti-inflammatory activity, cardioprotection, TNF-α, IL-1β, p65 nuclear translocation
- MeSH terms
- Receptor for Advanced Glycation End Products, Animals, Anti-Inflammatory Agents, Diabetes Mellitus, Experimental, Male, Myocardium, RNA, Messenger, Streptozocin, NF-kappa B, Glycation End Products, Advanced, Rats, Sprague-Dawley, Oxidative Stress, Xanthones, Rats, Interleukin-1beta, Diabetic Cardiomyopathies, Diet, High-Fat
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