Objective. Ovarian torsion is a gynecological emergency that occurs mostly during the female reproductive years due to ovarian masses or surgical manipulation. This work aims to explore the probable protective effect of leptin on rat ovaries due to ischemia-reperfusion (IR) injury. Methods. Wistar albino rats were divided into four groups: 1) control group; 2) ovarian IR group (OVIR); 3) leptin group I [OVIR + leptin (10 µg/kg body weight, b.w.)]; and 4) leptin group II (OVIR + leptin (100 µg/kg b.w.)]. Serum levels of estradiol and anti-Mullerian hormone (AMH) were measured. Levels of oxidative stress and inflammatory markers in ovarian tissue were determined along with the expression of sirtuin 1 (Sirt1), nuclear erythroid factor-2 (Nrf2), cyclooxygenase-2 (COX-2), nuclear factor kappa (NF-κB), toll like receptor-4 (TLR4), and caspase-3. Results. Serum estradiol and AMH levels were decreased with increased expression of COX-2, TLR4, caspase-3, and NF-κB and decreased expression of Sirt1and Nrf2 in ovary of the OVIR group, which were improved by exogenous administration of both leptin doses. Conclusion. Leptin administration dose-dependently reduced the severity of OVIR injury via modulation of Sirt-1/Nrf2 and TLR4/NF-kB/caspase-3 signaling pathways. Thus, leptin may be used as an adjuvant measure to prevent ovarian damage and improve the outcomes. However, clinical studies are needed to evaluate these results in humans.

Melatonin reduced endometrial hyperplasia induced by estradiol in female albino rats

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.

Mammary gland hyperplasia is one of the risk factors for breast cancer. Till date, there is no study that has addressed the effect of hemin in this condition. Thus, this study was designed to evaluate the effect of the heme oxygenase 1 (HO-1) inducer (hemin) and its inhibitor (zinc protoporphyrin-IX) (ZnPP-IX) on mammary gland hyperplasia (MGH) induced by estrogen and progesterone in adult albino rats. Forty adult female albino rats were divided into the control group, MGH group, MGH + Hemin group, and MGH + Hemin + ZnPP-IX group. Serum levels of estradiol and progesterone were measured. Breast tissues were taken for estimation of oxidative, inflammatory, and apoptotic markers. Mammary gland histology was performed, and expression of Ki-67, Beclin, and P53 in breast tissue was also measured. Estrogen and progesterone administration induced hyperplasia of cells lining the ducts of the breast tissues associated with increased diameter and height of the nipples as well as increased oxidative stress markers, inflammatory markers, antiapoptotic markers, and cell autophagy. Hemin administration during induction of MGH can reverse all the affected parameters. Then, these effects were abolished by ZnPP-IX administration. We concluded that hemin administration can antagonize the cell stress induced by estrogen and progesterone and protect against the development of mammary gland hyperplasia via modulation of Nrf2/HO-1 and NF-κB pathways. Graphical Abstract