ABSTRACT
Objective To investigate the effect of mifepristone on the expression of β-endorphin in the ectopic focus of adenomyosis.Methods The expression of β-endorphin was measured by the immunochemistry method.Results During proliferative phase and secretory phase,the β-endorphin of mild dysmenorrhea were higher than that of midrange dysmenorrhea(t=2.672,2.711,all P＜0.05),the β-endorphin of midrange dysmenorrhea was higher than that of severe dysmenorrhea(t=2.341,2.365,all P＜0.05),the difference was significant.After being cured by mifepfistone,the expression of β-endorphin in the ectopic focus of adenomyosis was higher than that of control group (t=2.478,2.356,all P＜0.05),still lower than that of normal endometrial tissue,(t=2.123,2.233,all P＜0.05),the difference was significant.Conclusion The expression of β-endorphin in the ectopic focus of adenomyosis decreased significandy accompanied with the aggravation of the dysmenorrhea,and the mifepfistone could upregulate the β-endorphin and relieve the dysmenorrhea.
ABSTRACT
Objective To investigate the effect and significance of cinobufagin on the expression of survivin of HHUA cells in the endometrial carcinoma cultured in vitro. Methods HHUA cells of endometrial carcinoma were cultured in vitro. After being intervened by cinobufagin with different concentration, the expression of survivin was measured by RT-PCR and the cellular apoptosis was tested by flow cytometry. Results In the control group: mRNA expression of survivin of HHUA cells in endometrial carcinoma was (1.22±0.23), cellular apoptutic rate was (2.31± 0.98)%; cinobufagin of 0.25 mg/ml didn't affect the survivin and cellular apoptotic rate (q=2.89, P>0.05: q=3.12, P>0.05) ; after being exposed to einobufagin of 2.5 mg/ml, the expression of survivin was (0.73± 0.26), and cellular apoptotic rate was (26.50± 6.36) %, with all of these data being different from the control group significantly (q=5.68, P<0.05; q= 10.23, P<0.05) ; the actions of cinobufagin of 25 mg/ml on mRNA expression of survivin and apoptotic rate were similar to cinobufagin of 2.5 mg/ml (q=3.49, P>0.05; q=4.35, P>0.05) . Conclusion Cinobufagin of 2.5 mg/ml inhibit the mRNA expression of survivin and proliferation of HHUA cells in endometrial carcinoma.
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The P85 regulatory subunit protein and gene expression and P110 catalylic subunit activity of phosphatidylinositol 3-kinase (PI-3K) were investigated in adipose tissue of patients with gestational diabetes mellitus (GDM) in order to explore the molecular mechanisms of insulin resistance (IR) of GDM. Samples from patients with GDM (n=50), and controls (n=50) were collected. Fasting insulin (FIN) was determined by radioimmunoassay. Fasting plasma glucose (FPG) was measured by oxidase assay. Western blot technique was used to detect the levels of PI-3K P85 subunit in adipose tissues of patients with GDM. The mRNA expression of PI-3K P85 subunit was detected by reverse transcription polymerase chain reaction (RT-PCR) method in the adipose tissue. PI-3K activity was examined by immunoprecipitation, thin-layer chromatography and gamma scintillation counting. The results were analyzed statistically. It was found that the levels of FPG, FIN and HOMA-IR in GDM group were significantly higher than those in control group (all P0.05). PI-3K activity was significantly decreased to 82.89% in GDM group as compared with control group (P<0.01) and negatively correlated with HOMA-IR (r=-0.75, P<0.01). It was concluded that PI-3K in GDM patients may be involved in the insulin signaling pathway, resulting in IR of GDM.
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The relationship between the expression of resistin in polycystic ovary syndrome (PCOS) and insulin resistance was investigated. The plasma resistin concentrations in 35 patients with PCOS and 40 controls were measured by ELISA. Luteinizing hormone (LH), follicle-stimulating hormone (FSH), and fasting insulin (FIN) were tested by radioimmunoassay. Insulin resistance index (HOMA-IR) was calculated. Fasting plasma glucose (FPG) was determined by oxidase test. Western blot and reverse transcriptase PCR (RT-PCR) methods were used to detect the expression of resistin in adipose tissues. The levels of plasma resistin, LH, LH/FSH and FIN and HOMA-IR in patients with PCOS were significantly higher than those in control group (all P<0.05). Plasma resistin was correlated positively with FPG, FIN, HOMA-IR, LH and LH/FSH (r=0.56, 0.60, 0.65, 0.48, and 0.42 respectively). Resistin protein and mRNA expression levels in patients with PCOS were significantly higher than those in normal tissues (all P<0.01). It was concluded that resistin might be involved in the pathogenesis of insulin resistance of PCOS.
ABSTRACT
Objegtive To investigate the effect and significance of cinobufagin on the expression of CD44s in ovarian carcinoma 3AO cells cultured in vitro.Methods Ovarian carcinoma 3AO cells were cultured in vitro;after the intervention of tinobufagin with different concentration,the expression of CD44s was measured by RT-PCR,and the cellular apoptosis was tested by flow cytometry.Results Ovarian carcinoma 3AO cells expressed CD44S mRNA of 1.3±0.1 and the cellular apoptofic rate was(2.31±0.98)%:0.25 mg/ml cinobufagin did not affect CD44s mRNA and cellular apoptofic rate(P ＞0.05):when 2.5 mg/ml cinobufagin was intervened,the expression of CD44s mRNA was 1.0±0.1 and the cellular apoptotic rate Was(28.69±4.16)%,showing significant difference comparing with the control group of ovarian carcinoma 3AO ceils(P＜0.05):the intervention of 25 mg/ml cinobufagin was similar to that of 0.25 mg/ml cinobuhgin(P＞0.05).3AO cells.