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

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.