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1.
Am J Transl Res ; 15(2): 1271-1280, 2023.
Article in English | MEDLINE | ID: mdl-36915753

ABSTRACT

OBJECTIVE: To investigate the effects of letrozole combined with ethinylestradiol and cyproterone acetate tablets on serum sex hormones and lipid metabolism in patients with polycystic ovary syndrome (PCOS). METHODS: Clinical data of 152 PCOS patients in the First Affiliated Hospital of Guangxi University of Chinese Medicine from May 2019 to June 2021 were collected for a retrospective analysis. Among the patients, 73 treated with ethinylestradiol and cyproterone acetate tablets alone were seen as control group (CG), and the rest 79 with letrozole combined with ethinylestradiol and cyproterone acetate tablets were seen as observation group (OG). The treatment efficacy was observed, and the adverse reactions in the course of treatment were counted. The levels of luteinizing hormone (LH), follicle stimulating hormone (FSH), testosterone (T), estrogen (E2), total cholesterol (TC), triglyceride (TG), high-density lipoprotein (HDL) and low-density lipoprotein (LDL) were compared before and after treatment. The number of mature follicles, ovulation rate and pregnancy rate were assessed. Multivariate logistic regression analysis was used to detect the independent risk factors of ineffective efficacy. RESULTS: After the treatment, the total efficacy rate of the OG was higher than that of the CG (P<0.05); moreover, the levels of TC, TG, LDL, FSH, LH and T in OG were lower while HDL and E2 were higher (all P<0.05) than those of the CG. Also, the number of mature follicles, ovulation rate and pregnancy rate were higher in OG than those in the CG (all P<0.05). There was no obvious difference in the incidence of adverse reactions between the groups (P>0.05). Higher fasting glucose, higher Ferriman-Gallway hair score, single drug treatment regimen, higher systolic blood pressure, and lower E2 before treatment were independent risk factors for ineffective treatment efficacy. CONCLUSION: Letrozole combined with ethinylestradiol and cyproterone acetate tablets can enhance the treatment efficiency of PCOS and improve serum sex hormones and lipid metabolism in PCOS patients.

2.
J Recept Signal Transduct Res ; 40(1): 89-96, 2020 Feb.
Article in English | MEDLINE | ID: mdl-31971049

ABSTRACT

Objective: Endometrial carcinoma (EC) was the fourth female malignancies in developed countries. Given that the prognosis of EC is extremely poor, it is vital to investigate its pathogenesis and effective therapeutic targets. However, the mechanism of osthole in EC remains unknown.Materials and methods: Firstly, the different doses of osthole (0, 50, 100, and 200 µM) were used to treat the Ishikawa and KLE cells. The cell proliferation, apoptosis, and cell cycle were measured by cell counting kit-8 (CCK-8), Annexin V-FITC/PI, and cell cycle assays. The apoptosis-related protein levels were examined by western blot. The miR-424 levels in Ishikawa and KLE cells were assessed by quantitative RT-PCR (qRT-PCR). Also, the binding of miR-424 and cytoplasmic polyadenylation element binding protein 2 (CEPB2) was detected by the luciferase reporter assay.Results: In this study, the increasing dose of osthole inhibited proliferation and induced apoptosis of Ishikawa and KLE cells. Moreover, the increasing dose of osthole up-regulated miR-424 and down-regulated the expression of CPEB2. CPEB2 was proved to be the target gene of miR-424. Interestingly, the over-expression of CPEB2 could reverse the changes of osthole-induced proliferation and apoptosis of Ishikawa and KLE cells.Conclusions: In summary, we provided first evidences that osthole inhibited proliferation and induced apoptosis through up-regulating miR-424 to inhibit expression of CPEB2 in EC. Our findings indicated that osthole might act as a novel and potential therapeutic agent for the treatment of EC.


Subject(s)
Apoptosis/drug effects , Coumarins/pharmacology , Endometrial Neoplasms/genetics , Endometrial Neoplasms/pathology , Gene Expression Regulation, Neoplastic/drug effects , MicroRNAs/genetics , RNA-Binding Proteins/metabolism , Up-Regulation/genetics , Base Sequence , Cell Line, Tumor , Cell Proliferation/drug effects , Coumarins/chemistry , Female , Humans , RNA-Binding Proteins/genetics , Up-Regulation/drug effects
3.
Horm Metab Res ; 52(1): 49-57, 2020 Jan.
Article in English | MEDLINE | ID: mdl-31945791

ABSTRACT

Polycystic ovarian syndrome (PCOS) is the most common endocrine disease that causes reproductive abnormalities in fertile women. It is closely related to the persistent anovulatory, insulin resistance, and high androgen. However, the molecular mechanisms underlying the pathological development of PCOS are still unclear. In this study, we aimed to explore the distinctive metabolic patterns in insulin combined with human chorionic gonadotrophin induced PCOS. The dynamic changes of endogenous metabolites in the development of PCOS were studied using untargeted metabolomic approaches based on nuclear magnetic resonance. The results showed that the degree of PCOS disorder metabolites at different periods was not exactly the same. Twelve significantly differential endogenous metabolites from different time points were selected as potential biomarkers relate to pathological process of PCOS. Among them, six metabolites showed a good diagnostic accuracy with PCOS model. The arginine and proline metabolic pathway was considered as one of the most crucial pathways that affects occurrence and development of PCOS. In addition, IRS-1, Akt, PI3K, IκB, and NF-κB (p65) were significantly changed in the ovary tissue of PCOS rats, which revealed that the IRS-1-PI3K/Akt and NF-κB signal pathway may be involved in the development of PCOS. This study demonstrated that metabolomic analysis is a powerful tool for providing novel insight into understanding the pathogenesis of PCOS and provide a basic reference for the diagnosis of PCOS at the onset stage.


Subject(s)
Polycystic Ovary Syndrome/urine , Urine/chemistry , Animals , Female , Humans , Insulin Receptor Substrate Proteins/genetics , Insulin Receptor Substrate Proteins/metabolism , Metabolomics , Phosphatidylinositol 3-Kinases/genetics , Phosphatidylinositol 3-Kinases/metabolism , Polycystic Ovary Syndrome/genetics , Polycystic Ovary Syndrome/metabolism , Proton Magnetic Resonance Spectroscopy , Rats , Rats, Sprague-Dawley , Transcription Factor RelA/genetics , Transcription Factor RelA/metabolism
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