Polycystic ovary syndrome (PCOS), the most common female endocrine disease that causes anovulatory infertility, still lacks promising strategy for the accurate diagnosis and effective therapeutics of PCOS attributed to its unclear aetiology. In this study, we determined the abnormal reduction in circPSMC3 expression by comparing the ovarian tissue samples of PCOS patients and normal individuals. The symptom relief caused by up‐regulation of circPSMC3 in PCOS model mice suggested the potential for further study. In vitro functional experiments confirmed that circPSMC3 can inhibit cell proliferation and promote apoptosis by blocking the cell cycle in human‐like granular tumour cell lines. Mechanism study revealed that circPSMC3 may play its role through sponging miR‐296‐3p to regulate PTEN expression. Collectively, we preliminarily characterized the role and possible insights of circPSMC3/miR‐296‐3p/PTEN axis in the proliferation and apoptosis of KGN cells. We hope that this work provides some original and valuable information for the research of circRNAs in PCOS, not only to better understand the pathogenesis but also to help provide new clues for seeking for the future therapeutic target of PCOS.
BackgroundThe current guideline for oxytocin regimens in the abnormal labor of delivery is continuous infusion. The objective of the present study was to compare effects and safety measures of various available regimens of oxytocin in abnormal labor delivery.Material/MethodsIn this clinical experimental study, a total of 900 pregnant women admitted for delivery were randomized into 5 group with 162 each. Pregnant women received oxytocin as continuous administration of 16 mU/min (Group I), 1 mU/min (group II), 4 mU/min (group III), 5 mU/min quarter-hourly (group IV), and through a syringe pump (group V). Measurement of the expense of delivery, the ratio of the instrumental delivery, and the other secondary outcome measures was performed to find the best regimen of oxytocin. The 2-tailed paired t test and Mann-Whitney U test following Dunnett’s multiple comparison tests were used at 95% confidence level.ResultsPulsatile delivery had least risk of instrumental delivery as compared to continuous infusion (p<0.0001, q=6.663) and normal-frequency low-dose (p<0.0001, q=5.638) of oxytocin. The time required from infusion to delivery was longer for group II (p=0.001, q=2.925), group IV (p<0.0001, q=4.829), and group V (p<0.0001, q=41.456) than for group I. The expense of delivery was: group I < group II < group IV < group III < group V.ConclusionsHigh-dose and pulsatile preparation of oxytocin had reduced risks of operative delivery vs. continuous administration.
Polycystic Ovary Syndrome (PCOS) is a gynecologic disorder with unsatisfactory treatment options. Hyperandrogenism and insulin resistance (IR) are two symptoms of PCOS. The majority of PCOS patients (approximately 50% to 70%) have IR and moderate diffuse inflammation of varying degrees. We investigated in-vitro and in-vivo effects of naringenin, morin and their combination on PCOS induced endometrial hyperplasia by interfering with the mTORC1 and mTORC2 signaling pathways. The vaginal smear test ensured the regular oestrous cycles in female rats. Serum cytokines (TNF-α & IL-6) were assessed using the ELISA test, followed by in-vivo and in-vitro determination of prominent gene expressions (mTORC1& C2, p62, LC3-II, and Caspase-3 involved in the inflammatory signaling mechanisms through RT-PCR, western bloting, or immunohistochemical analysis. In addition, the viability of naringenin or morin treated cells was determined using flow cytometry analysis. The abnormal oestrous cycle and vaginal keratosis indicated that PCOS was induced successfully. The recovery rate of the oestrous cycle with treatments was increased significantly (P<0.01) when compared to the PCOS model. Narigenin, morin, or a combination of the two drugs substantially decreased serum insulin, TNF-α, IL-6 levels with improved total anti-oxidant capacity and SOD levels (P<0.01). Treatments showed suppression of HEC-1-A cells proliferation with increased apoptosis (P<0.01) by the upregulation of Caspase-3 expression, followed by downregulation of mTORC, mTORC1, and p62 (P<0.01) expressions with improved LC3-II expressions (P<0.05) respectively. The histological findings showed a substantial increase in the thickness of granulose layers with improved corpora lutea and declined the number of cysts. Our findings noticed improved inflammatory and oxidative microenvironment of ovarian tissues in PCOS treated rats involving the autophagic and apoptotic mechanisms demonstrating synergistic in-vitro and in-vivo therapeutic effects of treatments on PCOS-induced endometrial hyperplasia.
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