An Experimental Study on The Oxidative Status and Inflammatory Levels of A Rat Model of Polycystic Ovary Syndrome Induced by Letrozole and A New High-Fat Diet

一项关于来曲唑和新型高脂饮食诱导的多囊卵巢综合征大鼠模型氧化状态和炎症水平的实验研究

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Abstract

BACKGROUND: Although there are numerous animal models of polycystic ovary syndrome (PCOS), they often fail to accurately replicate the reproductive and metabolic phenotypes associated with PCOS. The objective of this study is to assess oxidative status and inflammatory levels in a rat model of PCOS subjected to a new high-fat diet (HFD) in combination with letrozole. MATERIALS AND METHODS: In this experimental study, mature, six-week-old female Sprague-Dawley rats (n=20) were divided into four groups: control (standard diet); letrozole (letrozole plus a standard diet); HFD; and letrozole+HFD. After 16 weeks, the rats underwent vaginal smear analysis, measurement of hormonal and lipid profiles, and an oral glucose tolerance test (OGTT). Ovarian tissue morphology, oxidative parameters, and inflammatory status were evaluated. RESULTS: The experimental groups exhibited anoestrus profiles in the vaginal smears and abnormal ovarian morphology, which was not observed in the control group. Steroid hormone levels were significantly higher in the letrozole+HFD group compared to the other groups (P=0.00). The experimental groups also showed abnormal glucose levels and lipid metabolism. The relative expression levels of inflammatory genes were significantly elevated in the experimental groups compared to the control group (P=0.00), and the letrozole+HFD group exhibited the highest expression level (P=0.00). The HFD, letrozole, and letrozole+HFD groups demonstrated significantly increased levels of malondialdehyde (MDA) and reactive oxygen species (ROS), while the levels of enzymatic antioxidants were significantly reduced compared to the control group (P=0.00). CONCLUSION: The combination of a new HFD and letrozole treatment induces inflammation and oxidative stress (OS) in a rat model of PCOS. This model accurately exhibits abnormal metabolic phenotypes and disruptions in hormonal profiles associated with PCOS.

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