Investigation of the effects of Quince jelly, Thymoquinone and Hesperidin in rats with Endometriosis model

Aim: To examine efficacy of protective effect of Quince gel (AJ), Hesperidin (HES) and Thymoquinone (TIM) against damage to uterine mucosa in P13K/AKT, mTOR, MAPK signaling pathways in Endometriosis (EM) model created by effect of estradiol benzoate (EB) by biochemical, histopathological immunohistochemical and ultrastructural methods. Materials and methods: For 7 days, 3 µg/kg EB was dissolved in 5% corn oil and given subcutaneously to rats. 6 groups was divided as Sham, EM, EM+AJ, EM+AJ+TIM, EM+AJ+HES and EM+AJ+HES+TİM. 2cc AJ+30 mg/kg HES and 50 mg/kg TIM were administered through vagina for 21 days. MDA, MPO, GSH-Px, SOD, CAT values were analyzed from blood samples. Uterine tissue was taken for histological, immunohistochemical, western blot and electron microscopy. Results: After endometriosis, thinning of uterine epithel, hyperplasic nucleus, increased inflammatory cell infiltrations, vessel dilatation and congestion were observed. In AJ application, integrity of the epithelial structure was preserved, inflammation was reduced, mixture of TIM and HES was important for uterine mucosa. PI3K-Akt-mTOR-MAPK pathways, which increase after EM, are inhibited in AJ application, AJ+HES, AJ+TIM and AJ+HES+TIM application, they slow down both inflammation, cell degeneration and apoptosis. Due to the degeneration of epithelial cells after endometriosis, AJ+HES+TIM had a significant effect on the preservation of structural integrity in nucleus at the ultrastructural level and the mitochondria in the cytoplasm. Conclusion: Endometriosis is a disease due to multifactorial effect, TIM with AJ, can have an alternative effect to maintain cellular energy balance by regulating cellular growth and proliferation in treatment of the disease in which PI3K-Akt-mTOR and MAP kinase signaling pathways are important. Key words: Apoptosis; endometriozis; estradiol benzoate; hesperidin; quince jelly; thymoquinone