Objective To investigate the effect ofestrogen on osteoarthritis in female rats.Methods Forty female rats were divided into four groups. In group Ⅰ, the rats were not given any treatment as a control. Ingroups Ⅱ, Ⅲ and Ⅳ, the rats received fixing left knee joint on extension position. Meanwhile, therats received ovariectomy in group Ⅲ; ovariectomy and diethylstilbestrol treatment in group Ⅳ, respectively. After 4 weeks, histological observation and serum BGP examination were done.Results In groups Ⅱ, Ⅲ andⅣ, the levels of serum BGP were 3.50±0.39, 5.72±0.64 and 3.95±0.44, respectively. The pathologic grades of cartilage and synovium were 10.83±4.35 and 4.21±2.03; 15.32±3.42 and 7.62±3.42; and 12.65±2.73 and 5.46±1.23, respectively. Conclusion Estrogen may play an important role in delaying the development of osteoarthritis.
Objective To investigate the relationship between the level of testosterone and estradiol in serum and central serous chorioretinopathy (CSC).Methods The clinical data of 200 patients with active phase CSC who diagnosed by clinical manifestation, examination of fundus and fluorescence fundus angiography (FFA), were retrospectively analyzed. Two hundreds healthy people were collected as a control group. The blood of ulnar vein was collected and the method of magnetic homogeneous enzyme immunoassay was used to detect the level of testosterone and estradiol in serum of two groups. The results were analyzed statistically by t test.Results The values of testosterone and estradiol of male were all higher in CSC group than that in control group，the differences were statistical significance（t=2.804，2.913；P=0.010，0.008）；it was also higher in female（t=2.078，2.807；P=0.049，0.010）. The value of testosterone/estradiol of male was higher than that of female in CSC group，the difference was statistical significance(t=2.231，P=0.046).Conclusions The level of testosterone and estradiol in serum of CSC group increased obviously, especially the value of testosterone/estradiol. The increase of estradiol and testosterone/estradiol may be an etiological factor of CSC.
Objective To review the regulating effects of estrogen on endothel ial cell functions, the involved endothel ial progenitor cells (EPCs), and the related VEGF, and explore the mechanism of estrogen participating in new vesselformation on wound basement and wound heal ing. Methods Recent l iterature about biological effects of estrogen oncapillary vessel formation was reviewed. Results The formation of new vessel in the wound’s granulation tissue contained vasculogenesis and vascularization, and the new vessels could transport the oxygen and nutrient for the metabol ism of the local heal ing tissue. The estrogen effected vascular endothel ial cells through its receptors. Peripheral vascular EPCs differentiated into endothel ial cells and participated into the formation of new vessels. Estradiol exerted influences on the dynamics of vascular EPCs and the neovascularization. VEGF was a key mediator in the processes of estradiol regulating angiogenesis. Conclusion Understanding the molecular mechanisms that regulate vessel formation in wound heal ing, especially how estrogen modulates its receptor and angiogenic factor, may provide new approaches for managing wound heal ing.
The level of androgen receptor (AR), estrogen receptor (ER) and progesterone receptor (PR) of carcinoma and pericarcinoma tissue were determined in 30 cases of male hepatocellular carcinoma (HCC) patients operated by streptavidin peroxdase conjugated method, meanwhile used 20 patients with benign liver disease as a contrast group. The results showed that the positive rate of AR in tumor tisse was 80.0%, significantly higher than that in peritumor tissue (46.7%) and liver tissue of benign diseases (40.0%), Ｐ＜0.01, and there was no significantly difference between the latter two groups (Ｐ＞0.05). The positive rate of ER in carcinoma tissue (43.3%) was notably lower than that in pericarcinoma tissue (80.0%), Ｐ＜0.01. Statistically significantly difference wasn’t achieved in contrast with the benign diseases group (50.0%), Ｐ＞0.05. The positive rate of PR had no significantly difference among the three groups (Ｐ＞0.05). The authors suggest that sex hormone is related to initializing and developing of HCC by the action via its receptor, the level of AR and ER can be used as a prognosis determine index of HCC.
ObjectiveTo summarize the relevant studies of pharmacological mechanism of tamoxifen and its influence on ovary function in order to provide information and evidence for the therapy of breast cancer.
MethodsPapers published from January 1950 to January 2014, were retrieved in MedLine, OVID, CBM, CNKI databases using the keywords on tamoxifen, drug metabolism, ovary, sex hormone, etc, 1286 papers were retrieved in English literatures, and 621 in Chinese literatures. Criteria of paper adoption:①The clinical and basic studies about metabolism of tamoxifen, metabolic effect of tamoxifen, and gene polymorphism of CYP2D6.②The role played by estrogen receptor and protein cofactors in tamoxifen effect.③The clinical and basic studies about tamoxifen induced ovulation, caused endometrial thickening, changed sex hormone levels. According to the above criteria, 152 papers were selected, and 77 papers out of them were finally analyzed and reviewed.
Results①The tamoxifen metabolite 4-OH-N-tamoxifen was the main working component, the decreased levels could predict the poor prognosis.②The CYP2D6 gene polymorphism could affect the metabolic effect of tamoxifen and the therapeutic effect of patients with breast cancer.③The metabolic effect of tamoxifen needed the participation of the estrogen receptors and protein cofactors.④Tamoxifen could affect the reproductive system function through the estrogen receptor of H-P-O axis, ovary, and endometrium.
ConclusionsMetabolic effect of tamoxifen is regulated by gene, it could affect reproductive system functions through estrogen receptor. the mechanism that tamoxifen cowld affect the hormone levels and wherther it could reflect the ovarian function by monitering the hormone levels continuously for patients with breast cancer need to be researched.
ObjectiveTo summarize progression of growth factor receptor (GFR) signaling pathway in endocrineresistant breast cancer. Method Literatures about mechanisms of GFR signaling pathway in the development of endocrineresistant breast cancer were reviewed.
ResultsThe crosstalk between GFR and estrogen receptor (ER) signaling pathway had been reported to be involved in the development of endocrine-resistant breast cancer. Interrupting this signaling pathway could overcome endocrine therapy resistance. Many clinical trails had shown that the utilizing endocrine therapy combined with GFR inhibitors could obviously increase the survival rate of patients with breast cancer.
ConclusionSeveral agents targeting GFR signaling pathways show a great potential for treatment of patients with breast cancer.
Objective To review the mechanisms of cholesterol gallstones caused by female hormone so as to explore new treatments to prevent gallstones associated with estrogen and progesterone. Methods The literatures on gallstones related with female hormone were reviewed and the mechanisms of cholesterol gallstones were summarized. Results The cholesterol gallstones mechanisms was affected by estrogen through genomic effects，and the nucleation of cholesterol was promoted by estrogen through nongenomic，which resulted in the formation of cholesterol gallstones. And the bile empty dysfunction associated with estrogen through nongenomic effects was also the reason of cholesterol gallstone formation. The G proteins α subunit responsible for the motility of gallbladder were disrupted by progesterone through genomic effects，and the ionic channels and signal transduction were also interfered through nongenomic pathway，which impaired the contraction of gallbladder. However，the nongenomic effects might not play an important role in the gallstones formation caused by progesterone. Conclusions The mechanisms of cholesterol gallstones formation associated with female hormone are complicated，the understanding of chelesterol gallstones formation mechanisms might be helpful to prevent gallstones associated with estrogen and progesterone.
Objective To investigate the correlation of the polymorphism of the estrogen receptor alpha gene Pvu II site and coronary heart disease (CHD) in Chinese population. Methods Such databases as CBM, CNKI, Wangfang database, VIP, MEDLINE, The Cochrane Library, EMbase, Springer, and Ovid were searched from their establishment date to November of 2010 to collect the case-control studies on the correlation of estrogen receptor alpha gene polymorphism Pvu II sites with coronary heart disease of the Chinese. The quality of included studies was evaluated, the available data was extracted, and then the RevMan5.0 software was used for Meta analyses. Results Nine case-control studies were included, involving 1 464 cases with coronary heart disease and 1 203 cases in the control group. The results of Meta-analyses showed that, as to the correlation of the polymorphism of ER alpha gene Pvu II site T/C and CHD, there was no significant difference in the risk of CHD between people with different genotypes, i.e. the C allele versus T allele (OR=0.95, 95%CI 0.77 to 1.17, P=0.63), genotype of (TC + CC) versus TT (OR=0.97, 95%CI 0.73 to 1.28, P=0.81), genotype of TC versus TT (OR = 0.93, 95%CI 0.68 to 1.26, P=0.64), genotype of CC versus TT (OR=0.86, 95%CI 0.57 to 1.31, P=0.49). Conclusion Estrogen receptor alpha gene polymorphism Pvu II site are not associated with the coronary heart disease in Chinese population.
Objective To explore the effect of interfering RNA (shRNA) on biological activity of A549 cells and tumor growth in nude mice after knockdown of estrogen receptor α (ERα) gene. Methods The ERα gene in A549 cells was knocked down by shRNA. RT-PCR and Western blot were used to detect the gene expression and protein expression after knockdown; colony formation experiment was used to detect the proliferation of cells, and RT-PCR was used to detect the expression of Ki-67 and PCNA; flow cytometry was used to detect apoptosis rate; transwell assay was used to detect cell invasion ability; Western blot was used to detect the expression of epithelial cadherin (E-cad) and neuropathic cadherin (N-cad) protein. The control group and A549 cells transfected with ERα-shRNA1 were injected subcutaneously in nude mice to construct transplanted tumors. Immunohistochemistry was used to detect the expression of Ki-67 and N-cad in tumor tissues. Results Compared with the control group, after transfection of ERα-shRNA1 and ERα-shRNA2, the mRNA and protein expressions of ERα were reduced significantly (P<0.05), and shRNA1 with high interference efficiency was used for subsequent experiments. Compared with the control group, the A549 cells were transfected with ERα-shRNA1, the colony formation rate was down-regulated significantly (P<0.05), the apoptosis rate was increased significantly (P<0.05), the expression of Ki-67 and PCNA were down-regulated significantly (P<0.05), the number of invasive cells was reduced significantly, the expression of E-cad was increased, and the expression of N-cad was decreased (P<0.05). The results of tumor formation in nude mice showed that interfering with ERα expression can significantly inhibit tumor growth (P<0.05), and down-regulate the rate of Ki-67 and N-cad positive cells (P<0.05). Conclusion Knockdown of ERα inhibits the proliferation and migration ability of NSCLC cells and the occurrence and development of transplanted tumors in nude mice.
