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Original Research Article | OPEN ACCESS

Mangiferin ameliorates insulin resistance in a rat model of polycystic ovary syndrome via inhibition of inflammation

Qiaohong Qian, Minjie Tang, Xinrong Li, Qi Cao , Zhiling Zhu

Department of Integrative Medicine, Obstetrics and Gynecology Hospital, Fudan University, Shanghai 200011, China;

For correspondence:-  Qi Cao   Email: qicao@fudan.edu.cn   Tel:+862133189900

Accepted: 27 December 2019        Published: 31 January 2020

Citation: Qian Q, Tang M, Li X, Cao Q, Zhu Z. Mangiferin ameliorates insulin resistance in a rat model of polycystic ovary syndrome via inhibition of inflammation. Trop J Pharm Res 2020; 19(1):89-94 doi: 10.4314/tjpr.v19i1.14

© 2020 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..

Abstract

Purpose: To examine the effect of mangiferin on insulin resistance (IR) in a rat polycystic ovary syndrome (PCOS) model.
Methods: The rat PCOS model was established via subcutaneous injection of 6 mg/kg of dehydroepiandrosterone (DHEA), and mangiferin was orally administered. Body and ovarian weights were recorded. Serum levels of glucose, insulin, and related inflammatory cytokines were evaluated by quantitative real-time polymerase chain reaction (qRT-PCR) and enzyme-linked immunosorbent assay, while the expression levels of key proteins were analyzed by western blotting.
Results: DHEA significantly increased ovarian weight and the ratio of ovarian weight/body weight (p < 0.001), while mangiferin treatment decreased them (p < 0.001). Mangiferin also lowered DHEA-induced enhancements in serum glucose and insulin levels (p < 0.001). The mRNA and, expression and concentrations of inflammatory cytokines (interleukin-6(IL-6), interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α)) were also significantly reduced by mangiferin treatment (p < 0.001). Furthermore, mangiferin suppressed phosphorylation of nuclear factor-kappa B (NF-κB) but increased the phosphorylation of protein kinase B (AKT, p < 0.001).
Conclusion: These results reveal that mangiferin not only decreases inflammatory cytokine levels by regulating NF-κB signaling pathway but also ameliorates IR in a rat PCOS model via regulating AKT signaling pathway. Thus, mangiferin is a potential therapeutic strategy for the management of PCOS.

Keywords: Polycystic ovary syndrome, Mangiferin, Inflammation, Insulin resistance, NF-_4;B, AKT

Impact Factor
Thompson Reuters (ISI): 0.523 (2021)
H-5 index (Google Scholar): 39 (2021)

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