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

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.

Keywords:

• Diabetes
• endometrium
• rat
• sodium hydrosulphide
• DL-propargylglycine

Author contributions

Dr Heba A. Abdel-Hamid performed the research protocol, the experiment, collection and analysis of results, and wrote the manuscript. Dr Manar Fouli Gaber Ibrahim performed, wrote, and analysed the histopathology part and the immunohistochemistry sections. Dr Heba Marey performed and wrote the RT-PCR experiment. All authors revised the final version of the manuscript and agreed on its submission and publication.

Disclosure statement

No potential conflict of interest was reported by the author(s).

Data availability statement

The data that support the findings of this study are available on request from the corresponding author. The data are not publicly available due to privacy or ethical restrictions.