estradiol-3-benzoate and Endometrial-Hyperplasia

The diagnosis of uterine dysfunction (endometrial hyperplasia) is on the rise. The available treatment is quite expensive and associated with some side effects. The therapeutic potential of natural products is now being explored, as they are easily available with little or no side effects.. This study aims to investigate the potential therapeutic effect of chloroform fraction of methanol extract of. Thirty-six rats were randomly divided equally into six groups. These included control group, CFDC: (100 mg/kg), CFDC: (200 mg/kg), EB: (2 mg/kg), EB + CFDC (100 mg/kg), and EB + CFDC (200 mg/kg). Endometrial hyperplasia (EH) was induced by intraperitoneal injection of EB. The levels of estrogen (E2), progesterone (PG), Follicle stimulating hormone (FSH), Luteinizing hormone (LH), Malondialdehyde (MDA), Superoxide dismutase (SOD), and Glutathione peroxidase (GSH-Px) activities were determined using ELISA technique. The uterine histological assessment and immunohistochemical expression levels of estrogen receptor, Ki-67, cytochrome c, and caspase 3 were carried out.. EH was severely expressed in the uterine section of EB-treated rats. However, CFDC administration improved the pathological features of the animal model. The sex hormones levels were increased in the EB-treated group, which were significantly reduced by CFDC. The antioxidant indices were also restored by CFDC. Immunoexpression levels of ERα and Ki-67 were downregulated while cytochrome c and caspase 3 were upregulated by CFDC.. This study suggests that CFDC contains phytochemicals that can protect against EB-induced EH via modulation of hormonal signaling, apoptotic machinery, and oxidative indices.

Topics: Animals; Antioxidants; Caspase 3; Chloroform; Cytochromes c; Endometrial Hyperplasia; Estradiol; Female; Humans; Ki-67 Antigen; Rats; Receptors, Estrogen

Early detection and treatment of endometrial hyperplasia (EH) is mandatory for endometrial cancer prevention. Several bioactive agents of plant origin have been shown to elicit their chemotherapeutic effect against tumors and cancer via induction of mitochondrial permeability transition(mPT) pore opening. This research was therefore aimed at evaluating the potential chemopreventive effect of methyl palmitate (MP), on estradiol benzoate(EB)-induced EH, looking at the mitochondrial-mediated pathway and other possible mechanisms of action. Mitochondria were isolated using differential centrifugation. The mPT pore, mitochondrial ATPase (mATPase) activity, lipid peroxidation and cytochrome c release were determined by standard methods using spectrophotometer. Uterine interleukin 1b, MDA levels and SOD, GSH activities, were determined using commercially available kits. The uterine histological and immunohistochemical assessment of estrogen receptor (ERα), IL-1b and caspas-3 were carried out. The fibroblast cell count density was determined using histomorphometry. At all the concentrations of MP used, there was no significant induction of mPT pore opening, neither any enhancement of mATPase activity nor release of cytochrome c when compared to the control. Similar pattern of results were recorded for the

Topics: Animals; Anti-Inflammatory Agents; Antioxidants; Cell Proliferation; Cytochromes c; Endometrial Hyperplasia; Endometrium; Estradiol; Estrogen Receptor alpha; Female; Fibroblasts; Interleukin-1beta; Lipid Peroxidation; Mitochondria; Mitochondrial Proton-Translocating ATPases; Oxidative Stress; Palmitates; Rats, Wistar; Signal Transduction

Endometrial hyperplasia (EH) is a common gynecological condition and may progress to carcinoma. We investigated the effect of diacerein (DIA) on estradiol benzoate (EB)-induced EH and atypia. DIA (50 mg/kg/day) was administered orally to rats for 4 weeks, in the presence or absence of EH induced by intramuscular injection of EB (60 μg/100 g) three times per week for 4 weeks. We measured levels of serum total cholesterol, uterine tissue malondialdehyde (MDA), total nitrites (NO

Topics: Animals; Anthraquinones; Anti-Inflammatory Agents; Endometrial Hyperplasia; Estradiol; Female; Interleukin-1beta; Rats; Rats, Wistar

To explore a new reliable method inducing an animal model similar to the morphology and apoptotic signaling pathways in endometrial hyperplasia patients.. After the rats were ovariectomized, estradiol benzoate (60 µg/​100 g) was intramuscularly injected on alternate days for 4 weeks. The morphology in the uterus was observed under a light microscope and by electron microscopy. The expression levels of survivin/caspase-3 and Fas/FasL were checked by immunohistochemistry, Western blotting and real-time polymerase chain reaction.. After the models were induced, the edema and hypertrophy in uteri were observed 4 weeks later. The glands in the endometrium had increased, indented hyperplasia of glandular cells appeared, and a pseudo-stratified phenomenon occurred. Under a transmission electron microscope, free ribosomes had markedly increased and the nucleus was enlarged in the cytoplasm. Compared with the control group, the expression of survivin increased (p < 0.05) while that of caspase-3 and Fas/FasL declined (p < 0.05).. In the rat model of endometrial hyperplasia induced by ovariectomy with pharmacological estrogen add-back treatment, survivin, caspase-3 and Fas/FasL signaling pathways play an important role in regulating the apoptosis of glandular cells in uteri.

Topics: Animals; Apoptosis; Blotting, Western; Caspase 3; Disease Models, Animal; DNA; Endometrial Hyperplasia; Estradiol; Fas Ligand Protein; fas Receptor; Female; Immunohistochemistry; Microscopy, Electron, Transmission; Microtubule-Associated Proteins; Ovariectomy; Random Allocation; Rats; Rats, Sprague-Dawley; Real-Time Polymerase Chain Reaction; Signal Transduction; Specific Pathogen-Free Organisms; Survivin

Cystic endometrial hyperplasia (CEH) was induced in the left uterine horns of 14 mature ovariectomised greyhound bitches with an intra-luminal silk suture (uterine irritant) and treatment with estradiol benzoate and megestrol acetate (to simulate stages of a normal canine estrous cycle). Right uterine horns served as suture-free controls. From Day 30 of simulated diestrus, bitches received treatments of suture removal (n = 4), progestagen withdrawal (n = 5) or both (n = 5). Necropsies were performed 3 or 9 weeks later. At 3 weeks, severe cystic endometrial hyperplasia was present in all (6/6) left horns and in no (0/6) right horns. At 9 weeks, the left horns in 5/6 of bitches subjected to progestagen-withdrawal had recovered (in varying degrees) from cystic endometrial hyperplasia, whereas no recovery was evident in the left horns of bitches (n = 2) that continued to receive progestagen. This study demonstrated that: (i) cystic endometrial hyperplasia was reversible upon withdrawal of progestagen; (ii) progestagen maintained cystic endometrial hyperplasia in the presence or absence of irritant; and (iii) persistent endometrial irritation in the absence of progestagen may not maintain cystic endometrial hyperplasia.

Topics: Animals; Dog Diseases; Dogs; Endometrial Hyperplasia; Estradiol; Estrous Cycle; Female; Histocytochemistry; Irritants; Megestrol Acetate; Ovariectomy; Progestins; Silk; Sutures