Hydrogen sulfide protects the endometrium in a rat model of type 1 diabetes via modulation of PPARγ/mTOR and Nrf-2/NF-κb pathways.

IF 2.5 4区医学 Q3 ENDOCRINOLOGY & METABOLISM

Archives of Physiology and Biochemistry Pub Date : 2024-04-29 DOI:10.1080/13813455.2024.2347239

Heba A Abdel-Hamid, Heba Marey, Manar Fouli Gaber Ibrahim

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Abstract

Diabetes is one of the leading causes of endometrial diseases in women. No study has addressed the influence of hydrogen sulphide (H₂S) donors on endometrial injury on top of type 1 diabetes. This research was conducted to study either the effect of sodium hydrosulphide (NaHS), the H₂S donor, or DL-propargylglycine (PAG), the inhibitor of endogenous H₂S production, on the endometrium of diabetic rats. A total of 40 female Wistar rats were separated into control group, diabetic group, diabetic group treated with NaHS and diabetic group treated with PAG. Serum levels of insulin, glucose, total cholesterol (TC) and triglycerides (TG) were assessed. Uterine tissue markers of oxidative stress, inflammation, apoptosis and cell proliferation were analysed. Diabetes-induced endometrial overgrowth associated with oxidative stress, inflammation and inhibition of apoptosis. NaHS administration reversed the previous conditions while PAG administration got them worse. We concluded that H₂S prevented endometrial overgrowth in a rat model of type 1 diabetes through modulation of PPARγ/mTOR and Nrf-2/NF-κB pathways.

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硫化氢通过调节 PPARγ/mTOR 和 Nrf-2/NF-κb 通路保护 1 型糖尿病大鼠模型的子宫内膜。

糖尿病是导致女性子宫内膜疾病的主要原因之一。目前还没有研究探讨硫化氢（H2S）供体对 1 型糖尿病子宫内膜损伤的影响。本研究旨在研究 H2S 供体硫化氢钠（NaHS）或内源性 H2S 生成抑制剂 DL-丙炔基甘氨酸（PAG）对糖尿病大鼠子宫内膜的影响。将 40 只雌性 Wistar 大鼠分为对照组、糖尿病组、NaHS 治疗糖尿病组和 PAG 治疗糖尿病组。对血清中的胰岛素、葡萄糖、总胆固醇（TC）和甘油三酯（TG）水平进行了评估。分析了子宫组织氧化应激、炎症、细胞凋亡和细胞增殖的标志物。糖尿病诱发的子宫内膜增生与氧化应激、炎症和细胞凋亡抑制有关。服用 NaHS 可逆转之前的情况，而服用 PAG 则会使情况恶化。我们的结论是，H2S 通过调节 PPARγ/mTOR 和 Nrf-2/NF-κB 通路，防止了 1 型糖尿病大鼠模型中的子宫内膜过度增生。

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来源期刊

Archives of Physiology and Biochemistry ENDOCRINOLOGY & METABOLISM-PHYSIOLOGY

CiteScore

6.90

自引率

3.30%

发文量

期刊介绍： Archives of Physiology and Biochemistry: The Journal of Metabolic Diseases is an international peer-reviewed journal which has been relaunched to meet the increasing demand for integrated publication on molecular, biochemical and cellular aspects of metabolic diseases, as well as clinical and therapeutic strategies for their treatment. It publishes full-length original articles, rapid papers, reviews and mini-reviews on selected topics. It is the overall goal of the journal to disseminate novel approaches to an improved understanding of major metabolic disorders. The scope encompasses all topics related to the molecular and cellular pathophysiology of metabolic diseases like obesity, type 2 diabetes and the metabolic syndrome, and their associated complications. Clinical studies are considered as an integral part of the Journal and should be related to one of the following topics: -Dysregulation of hormone receptors and signal transduction -Contribution of gene variants and gene regulatory processes -Impairment of intermediary metabolism at the cellular level -Secretion and metabolism of peptides and other factors that mediate cellular crosstalk -Therapeutic strategies for managing metabolic diseases Special issues dedicated to topics in the field will be published regularly.