ABSTRACT
To investigate the effect of placental isoferritin (PLF) on mouse embryo development in vitro, mice 2-cell embryos were co-cultured with human first trimester decidual cells at different concentrations of PLF in vitro. The following changes of the above system were observed under an invert microscope and the number of embryos were recorded and the embryos were classified. The results showed there was no significant difference in the percentage of embryos development to 4-cell, 8-cell and morula (P>0.05). PLF at the doses of 10 and 100 U/mL significantly enhanced more embryos development to the blastocyst and hatching blastocyst (P0.05). It was concluded that PLF at the concentration of 10-100 U/mL had no significant effects on the early development of mice embryos, however, PLF could promote the growth, differentiation, and hatching of preimplantation blastocysts.
Subject(s)
Coculture Techniques , Decidua/cytology , Embryo, Mammalian/cytology , Embryo, Mammalian/drug effects , Embryo, Mammalian/embryology , Embryonic Development/drug effects , Ferritins/isolation & purification , Ferritins/pharmacology , Placenta/chemistry , Tissue Culture TechniquesABSTRACT
To investigate the effect of placental isoferritin (PLF) on mouse embryo development in vitro, mice 2-cell embryos were co-cultured with human first trimester decidual cells at different concentrations of PLF in vitro. The following changes of the above system were observed under an invert microscope and the number of embryos were recorded and the embryos were classified. The results showed there was no significant difference in the percentage of embryos development to 4-cell,8-cell and morula (P>0.05). PLF at the doses of 10 and 100 U/mL significantly enhanced more em-bryos development to the blastocyst and hatching blastocyst (P<0.05). PLF at the dose of 1000 U/mL depressed more embryos development from 2-cell to hatching blastocyst, meanwhile such phenom-ena as cell degeneration and irregular cleavage were observed in part of embryos, but there was no significant difference in statistics (P>0.05). It was concluded that PLF at the concentration of 10--100 U/mL had no significant effects on the early development of mice embryos, however, PLF could promote the growth, differentiation, and hatching of preimplantion blastocysts.
ABSTRACT
In order to explore the effects of metformin combined with cyproterone acetate (CPA) on the clinical features, endocrine and metabolism of the patients with polycystic ovarian syndrome (PCOS), 50 cases of non-obese PCOS were randomly subjected to CPA (CPA treatment group, n = 25) and CPA+ metformin (n = 25) treatment for 6 months. Before and after treatment the body mass index (BMI), waist : hip ratio (WHR), ovarian volume, serum gonadotrophin, androgen and sex hormone-binding globulin (SHBG) levels, and fasting lipid, glucose and insulin levels were measured. The results showed that all of the parameters in two groups were similar before treatment. After treatment for 6 months in the CPA+ metformin group, BMI and WHR were significantly decreased, while insulin sensitivity was significantly decreased as Compared with those before treatment. In CPA group, no significant changes were found before and after treatment. Combined use of CPA and metformin could result in the reduction of serum androstenedione and increases of serum SHBG levels as compared with the CPA treatment alone. It was concluded that combined use of CPA and metformin could improve the insulin sensitivity, and further suppress the hyperandrogenism in non-obese women with PCOS.
Subject(s)
Androgen Antagonists/therapeutic use , Androstenedione/blood , Body Mass Index , Cyproterone Acetate/therapeutic use , Drug Therapy, Combination , Hypoglycemic Agents/therapeutic use , Insulin Resistance , Metformin/therapeutic use , Polycystic Ovary Syndrome/drug therapyABSTRACT
In order to explore the effects of metformin combined with cyproterone acetate (CPA) on the clinical features, endocrine and metabolism of the patients with polycystic ovarian syndrome (PCOS), 50 cases of non-obese PCOS were randomly subjected to CPA (CPA treatment group, n=25) and CPA+metformin (n= 25) treatment for 6 months. Before and after treatment the body mass index (BMI), waist: hip ratio (WHR), ovarian volume, serum gonadotrophin, androgen and sex hormone-binding globulin (SHBG) levels, and fasting lipid, glucose and insulin levels were measured. The results showed that all of the parameters in two groups were similar before treatment. After treatment for 6 months in the CPA+ metformin group, BMI and WHR were significantly decreased, while insulin sensitivity was significantly decreased as compared with those before treatment. In CPA group, no significant changes were found before and after treatment. Combined use of CPA and metformin could result in the reduction of serum androstenedione and increases of serum SHBG levels as compared with the CPA treatment alone. It was concluded that combined use of CPA and metformin could improve the insulin sensitivity, and further suppress the hyperandrogenism in non-obese women with PCOS.
ABSTRACT
To investigate the relationship between the insulin resistance (IR) of polycystic ovarian syndrome (PCOS) rat model induced by dehydroeplandrosterone (DHEA) and hormonal changes in the ovarium and the resistin mRNA levels in adipose tissue, 21-day-old female SD rats were divided into two groups in pairs. The rats in group 1 were injected daily (s.c.) with DHEA for up to 20 days and the rats in group 2 injected with oil at the same time. Ovarian weight, serum insulin levels and sex hormone levels in rat blood of both groups were determined. Oral glucose tolerance tests, light microscopic and electronic microscopic examination were performed. The levels of resistin mRNA in adipose tissue were measured by reverse transcription-polymerase chain reaction (RT-PCR). Our results showed that the ovarian weight in group 1 was greater than that in group 2 (P<0.05). The ovaria in group 1 showed multiple follicular cysts, The serum testeosterone and etrasdiol concentration were significantly higher in group 1 than those in group 2 (P<0.001 and P<0.05 respectively), so as the fasting serum glucose (P<0.001) and fasting serum insulin (P<0.05). The value of 1/FINS x FGC was significantly higher in group 1 than that in group 2 (P<0.001). Moreover, the resistin mRNA level of white adipose tissue in the DHEA-induced group was significantly higher than that in the control rats (P<0.05). It is concluded that the DHEA-induced PCOS rat models were similar to those of the patients with PCOS, and the IR was observed. Resistin secreted by adipose tissue may mediate IR in PCOS, and it is likely involved in the pathogenesis and development of PCOS.
Subject(s)
Animals , Female , Rats , Adipose Tissue , Metabolism , Animals, Newborn , Dehydroepiandrosterone , Estradiol , Blood , Insulin Resistance , Polycystic Ovary Syndrome , Metabolism , RNA, Messenger , Genetics , Rats, Sprague-Dawley , Resistin , Genetics , Testosterone , BloodABSTRACT
To explore whether the imprinting status of IGF-2 in the malignant epithelial ovarian tumors is different from that in benign tumors, the target sequences (DNA and RNA) which contain a polymorphism site for ApaI restriction endonuclease digestion were amplified with PCR and RT-PCR methods. Then the PCR/RT-PCR products were digested by ApaI. The IGF-2 transcriptional pattern came out from the results of endonucleases digestion. Among the 36 cases of benign epithelial ovarian tumors, 20 were heterozygous for ApaI locus and all showed genomic imprinting. While in the malignant group, 22 were heterozygous for ApaI locus but six were found to lose imprinting. Significant differences existed between the two groups (P < 0.05). Loss of imprinting of IGF-2 may serve as a marker for differentiating the malignant ovarian cancers from the benign ones. In a new field of molecular genetics, our research provides an experimental basis for genetic diagnosis and treatment of the ovarian cancers.
Subject(s)
Female , Humans , Cystadenocarcinoma, Serous , Genetics , Cystadenoma , Genetics , Genomic Imprinting , Insulin-Like Growth Factor II , Genetics , Ovarian Neoplasms , GeneticsABSTRACT
To explore whether the imprinting status of IGF-2 in the malignant epithelial ovarian tumors is different from that in benign tumors, the target sequences (DNA and RNA) which contain a polymorphism site for ApaI restriction endonuclease digestion were amplified with PCR and RT-PCR methods. Then the PCR/RT-PCR products were digested by ApaI. The IGF-2 transcriptional pattern came out from the results of endonucleases digestion. Among the 36 cases of benign epithelial ovarian tumors, 20 were heterozygous for ApaI locus and all showed genomic imprinting. While in the malignant group, 22 were heterozygous for ApaI locus but six were found to lose imprinting. Significant differences existed between the two groups (P < 0.05). Loss of imprinting of IGF-2 may serve as a marker for differentiating the malignant ovarian cancers from the benign ones. In a new field of molecular genetics, our research provides an experimental basis for genetic diagnosis and treatment of the ovarian cancers.
Subject(s)
Cystadenocarcinoma, Serous/genetics , Cystadenoma/genetics , Genomic Imprinting , Insulin-Like Growth Factor II/genetics , Ovarian Neoplasms/geneticsABSTRACT
To investigate the expression and implication of survivin protein and mRNA in decidua and villus and the effects of mifepristone on its expression, survivin levels in decidua and villus collected from 15 normal early pregnant women and 15 early pregnant women pretreated with 150 mg mifepristone and 400 micrograms misoprostol were assessed by immuno-histochemical techniques and reverse transcriptional-polymerase chain reaction (RT-PCR). Our results showed that survivin proteins were stained in the cytoplasm of trophoblasts and decidual cells and in the nuclei of some of the decidual glandular epithelial cells. The expression was strongest in the trophoblasts and decidual glandular epithelial cells. The expression values in the villus and decidua were (14.56 +/- 2.44) and (10.46 +/- 2.81) respectively for normal pregnant and (8.45 +/- 2.08), (7.33 +/- 1.91) for those pretreated with mifepristone respectively (P < 0.05). The transcription of survivin mRNA in villus and decidua of those pretreated with mifepristone decreased significantly compared with those in the normal pregnant women (P < 0.05). It is concluded that survivin can be expressed in the decidua and villus and mifepristone inhibits its mRNA transcription and protein expression, which could possibly be one of the factors inducing decidual and villous apoptosis.
Subject(s)
Female , Humans , Pregnancy , Apoptosis , Chorionic Villi , Metabolism , Decidua , Metabolism , Gene Expression Regulation , Inhibitor of Apoptosis Proteins , Microtubule-Associated Proteins , Genetics , Mifepristone , Therapeutic Uses , Neoplasm Proteins , Proto-Oncogene Proteins c-bcl-2 , Genetics , RNA, Messenger , Genetics , Random Allocation , Reverse Transcriptase Polymerase Chain Reaction , Trophoblasts , MetabolismABSTRACT
In order to explore a potential indicator of predicting the occurrence and development of gestational trophoblastic tumor, the expression of c-erbB2 oncogene in human normal placenta, hydatidiform mole and choriocarcinoma was investigated. The expression of c-erbB2 was detected immunohistochemically by monoclonal antibody against the gene on the formalin-fixed paraffin sections of 21 hydatidiform moles, 21 invasive moles, 20 choriocarcinomas and 30 normal placentas. Results showed that the expression level of c-erbB2 was significantly higher in gestational trophoblastic tumor than in hydatidiform mole and normal placenta of midterm and term pregnancy (P < 0.05), while there was no significant difference between patients with gestational trophoblastic tumor of stage III, IV and those of stage I, II. It was demonstrated that overexpression of c-erbB2 may closely associated with malignant transformation of hydatidiform mole, not only providing important insight into pathogenesis of gestational trophoblastic tumor, but also having an important significance for the early diagnosis and early treatment of gestational trophoblastic tumor.
Subject(s)
Female , Humans , Pregnancy , Biomarkers, Tumor , Choriocarcinoma , Metabolism , Genes, erbB-2 , Hydatidiform Mole , Metabolism , Hydatidiform Mole, Invasive , Metabolism , Placenta , Metabolism , Receptor, ErbB-2 , Genetics , Uterine Neoplasms , MetabolismABSTRACT
Objective To further study the mechanism of maternal fetal immune tolerance Methods Chorioplacental tissues were obtained from different gestation stages of normal pregnancy Immuno histochemistry was used to investigate the expression of Fas Ligand (FasL) on the surfaces of human cytotrophoblasts Highly precise color image measure system for immuno histochemistry was used for quantitative analysis Results FasL were expressed on the surfaces of placental cytotrophoblasts throughout normal pregnancy FasL staining areas on cytotrophoblasts of the first trimester, second trimester and term were (91410?8328) ?m 2, (101 322?11 480) ?m 2 and (97461?10517) ?m 2 respectively; Average brightness FasL staining were 0 227?0 032 5, 0 261? 0 021, 0 145? 0 015; and integral brightness were 21 391? 4 636, 25 993? 6 231, 18 588? 3 897 respectively The differences among the first, second and term pregnancy stages were significant Conclusions Like many immune privileged sites, the maternal specific fas + T cell apoptosis induced by FasL on the maternal fetal interface might be one of the significant mechanisms of maternal fetal immune tolerance The expression of FasL on the surfaces of placental cytotrophoblasts plays an important role both in the maintenance of pregnancy and in the normal development of fetus
ABSTRACT
Objective To study the immunol pathological mechanism of PIH through the expressron of FasL of placental trophoblasts. Methods Immuno histochemistry were used to detect the expression of FasL of placental trophoblasts on moderate and severe PIH patients, HPIS was used to determine the quantity of FasL. The expression of PIH group was compared with that of the normal control group. Result The scale of FasL expression on PIH group (69.628 ?19.103 ?m 2 ) was significantly lower than that of control group(97.461?10.517 ?m 2), P