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褪黑素和甲状腺激素受体与雌激素受体 α 的差异表达和相互作用可改善来曲唑诱导的大鼠多囊卵巢综合征的卵巢功能。

Differential expression and interaction of melatonin and thyroid hormone receptors with estrogen receptor α improve ovarian functions in letrozole-induced rat polycystic ovary syndrome.

机构信息

Department of Zoology, Kalinga University, Raipur, India.

Department of Zoology, Guru Ghasidas Vishwavidyalaya, Bilaspur, India.

出版信息

Life Sci. 2022 Apr 15;295:120086. doi: 10.1016/j.lfs.2021.120086. Epub 2021 Oct 25.

Abstract

AIMS

The objective of the present study was to investigate the effect of melatonin and L-thyroxine (T4) on the expression of various receptors, and some metabolic, reproductive, and gonadotropic hormones in letrozole-induced polycystic ovary syndrome (PCOS) in rats.

MATERIAL AND METHODS

Assessment of gravimetric, hormonal profile and thyroid histology and relative expression of melatonin receptors (MT1, MT2) and estrogen receptor α (Erα) in thyroid and ovary, and type II iodothyronine deiodinase (Dio2) and thyroid hormone receptor α (TRα) in the ovary were performed using standard protocols.

KEY FINDINGS

A significant increase in thyroid follicles numbers was noted in the hyperthyroid rat. T4 treatment to PCOS showed the expected increment in the circulating level of triiodothyronine (T) and T. Melatonin and T4 treatment of PCOS rats resulted in a significant decrease in the circulating level of T and T. Hyperthyroid rats showed a decrement in plasma melatonin levels. However, T4 treatment to PCOS rats showed increased circulating melatonin levels, and a decrease in the circulating level of gonadotropins (LH and FSH), and testosterone. Melatonin treatment to PCOS-hyperthyroid rats resulted in the normal expression of ovarian and thyroid MT1 and ERα, receptors, which had been altered in PCOS and hyperthyroid rats, without any significant change in the MT2 receptor.

SIGNIFICANCE

The present findings suggest a fine interplay and cross-talk via melatonin and its two receptors with ERα, TRα, and Dioin thyroid and ovarian tissue during PCOS and hyperthyroidism pathogenicity.

摘要

目的

本研究旨在探讨褪黑素和 L-甲状腺素(T4)对来曲唑诱导的多囊卵巢综合征(PCOS)大鼠各种受体以及一些代谢、生殖和促性腺激素表达的影响。

材料和方法

采用标准方案评估体重、激素谱和甲状腺组织学,以及褪黑素受体(MT1、MT2)和甲状腺激素受体 α(TRα)在卵巢中的相对表达,以及Ⅱ型碘甲状腺原氨酸脱碘酶(Dio2)在卵巢中的相对表达。

主要发现

在甲状腺功能亢进的大鼠中,观察到甲状腺滤泡数量显著增加。T4 治疗 PCOS 导致循环三碘甲状腺原氨酸(T3)和 T4 水平升高。褪黑素和 T4 治疗 PCOS 大鼠导致循环 T3 和 T4 水平显著降低。甲状腺功能亢进大鼠的血浆褪黑素水平降低。然而,T4 治疗 PCOS 大鼠导致循环褪黑素水平升高,促性腺激素(LH 和 FSH)和睾酮水平降低。褪黑素治疗 PCOS-甲状腺功能亢进大鼠导致卵巢和甲状腺 MT1 和 ERα 受体的正常表达,这些受体在 PCOS 和甲状腺功能亢进大鼠中发生了改变,而 MT2 受体没有发生任何显著变化。

意义

本研究结果表明,在 PCOS 和甲状腺功能亢进的发病机制中,褪黑素及其两种受体与 ERα、TRα 和 Dio2 在甲状腺和卵巢组织中存在精细的相互作用和串扰。

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