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Effects of estradiol-17β on the giant freshwater prawn were observed in case of the embryonic tolerance, growth, development, survival rate, yolk adsorption, eye appearance, and muscular compactness. The methods were designed in two steps; those were the tolerance and the growth. In the two hours after spawning, embryos were immersed in 10, 50, 100, or 150 µg/ml estradiol-17β solution for two days, and the controls were treated with 15% artificial seawater. The tolerance was monitored in a separate experiment; they were immersed in 10, 50, 100, or 150 µg/ml estradiol-17β solutions showed that the mortality rate at 150 µg/ml estradiol-17β was 31.66%. The growth represented by yolk adsorption, hatching rate, and eye appearance. The results showed that the eyes appeared earlier than those of the controls. The survival rates were investigated in other experiments. The results showed that the highest survival rate was 48.16%, observed in the 50 µg/ml estradiol-17β treatment. Therefore, estradiol might accelerate the growth as indicated by the number of days for eye appearance being shorter period than in the control treatment. The eyes of the embryos treated with 50, 100, and 150 µg/ml estradiol-17β appeared on day 10, whereas those in the control were observed on day 16. Hatching rate was tending to high in 150 µg/ml estradiol-17β but those were not significance with the control. Yolk adsorption was found in treated embryo rather than those of the controls. The pattern of yolk cluster distribution was differing from the control. The muscle tissue was observed on day 20 after the histological process. The results showed that the bundles muscle cells were more compactness and were larger, denser, and stronger with increasing concentrations of estradiol-17β than that the controls. Therefore, estradiol-17β should be applied to stimulate growth and might be introduced with the feed to the prawn industry and manufacturing
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Objective:To explore the mechanisms of ERK in affecting estrogen receptor signaling pathway by investigating the changes of the expression levels of nuclear receptor co-activatorPCAF protein and wild-type P53 protein and their gene transcription in the process of estrogen promoting transformation of cell cycle and resisting apoptosis of breast cancer cell MCF-7 after inhibitting ERK. Methods:Estrogen receptor-positive breast cancer cells MCF-7 were divided into 17?-estradiol treatment group,17 ?-E2 + ERK inhibitor PD98059 treatment group,and the control group. The apoptosis of cell and cycle were analyzed by flow cytometry. The expression of phosphorylated ERK1/2 and PCAF protein and wild-type p53 were detected by Western blot.The expression of pcaf mRNA and wild-type p53 mRNA were detected by RT-PCR. Results:With phosphorylation inhibitor of ERK PD98059,the effect of 17?-estradiol in resisting apoptosis and prmoting transformation of MCF-7 cell cycle was reversed,and the rate of early apoptosis of MCF-7 cell was raised(P0.05).The protein expression level and gene transcription of wild-type P53 were reinforced (P
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Objective To investigate the effect of 17?-estradiol (E2) on the expression of hepatocyte growth factor (HGF) mRNA in the myocardial tissues in rats during myocardial ischemia-reperfusion (I/R) process, and explore the relationship between HGF mRNA expression and myocardial apoptosis. Methods Using the random number table, 40 male SD rats were divided into 2 groups (20 rats in each group) randomly, ischemia-reperfusion (control) group and E2 treatment group. Myocardial I/R models of rats were duplicated by ligating the left anterior descending coronary artery for 20 min then reperfusion for 30 min. The expression of HGF and the apoptosis of myocardiocytes were observed with RT-PCR, TUNEL and flow cytometry. Results At the points of cardiac ischemia for 20 min and reperfusion for 30 min, in the E2 treatment group, the expressions of HGF mRNA were significantly higher than corresponding points of the control group (P
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AIM: To investigate the relaxative characteristics of resveratrol(RES) and 17?-Estradiol(EST) on coronary arteries in dogs and its mechanism.METHODS: Rings of canine coronary arteries were suspended in organ baths containing Krebs-Henseleit solution,and then isometric tension was measured.RESULTS: Both RES and EST caused the does-response contractile curve of KCl in K-H solution and CaCl_2 in Ca~(2+)-free K-H solution shift rightward,and their sensitivies and the values of maximum contractions had been decreased.In the N?-L-nitro-arginine,Methylene Blue and Sodium Orthovanadate groups,the vasorelaxant effects of both estrogens were markedly attenuated(P(0.05)).CONCLUSION: Resveratrol and 17?-Estradiol relaxe vascular smooth muscle in an endothelium-dependent manner,and are not related to KATP channel.
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To compare the effect of intermittent parathyroid hormone (PTH) treatment with that of estrogen treatment on epiphyseal growth in ovariectomized rats, 46 Sprague-Dawley female rats aged 9-10 weeks (about 200-220 g) were either ovariectomized or sham operated. From 6 weeks after ovariectomy (ovx), rats were daily injected with subcutaneous human recombinant PTH (1-84)-dosed 30 micrograms/kg (the low dose PTH-treated group) or 300 micrograms/kg (the high dose PTH-treated group), 17 beta-estradiol (the 17 beta-estradiol-treated group, 30 micrograms/kg) or vehicle (the ovx-alone group), 5 times a week for 4 weeks. The decalcified sections of the distal femoral epiphyseal plate were analyzed on light microscopy after H&E stain, and the lengths of the zones of proliferation, maturing and hypertrophic chondrocytes were measured. The length of the growth plate, the zone of proliferation and the zone of hypertrophic chondrocyte in the ovx-alone group were significantly shorter than those of the sham-operated group. The treatment of 17 beta-estradiol speeded up the differentiation of cells from proliferating chondrocytes to maturing and hypertrophic chondrocytes even though the length of the growth plate was comparable to that of the sham-operated group. Both low and high dose PTH treatments increased the length of the growth plate, and those lengths were comparable to that of the sham-operated group. The fractions of proliferating, maturing and hypertrophic zone in the low dose PTH-treated group were also comparable to those of the sham-operated group. However, high dose PTH treatment slowed down the differentiation of cells from proliferating chondrocytes to maturing and hypertrophic chondrocytes to a greater extent, and therefore the fraction of proliferating chondrocytes of the high dose PTH-treated group was larger than that of the low dose PTH-treated group (73.8 +/- 1.8 Vs 63.3 +/- 1.3%, p < 0.005). From these results, we showed that intermittent PTH treatment could promote linear growth in the ovariectomized growing rat. We propose that PTH may be an alternative drug candidate for promoting linear growth of long bones without the risk for early closure of the growth plate.
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Femenino , Humanos , Ratas , Animales , Desarrollo Óseo/efectos de los fármacos , Ovariectomía , Hormona Paratiroidea/farmacología , Hormona Paratiroidea/administración & dosificación , Ratas Sprague-Dawley , Proteínas RecombinantesRESUMEN
Objective To explore the effects of octylphenol, an environmental contaminant with estrogenic activity, on the expression of apoptosis regulator gene bcl-2 mRNA in human breast cancer cell line MCF-7 and to compare its effects with 17?-estradiol (E 2). Methods MCF-7 cells were cultured in vitro and exposed to various concentrations of octylphenol and E 2 from 12 h to 120 h respectively. Total RNA was abstracted and the expression of bcl-2 mRNA was measured using reverse transcription polymerase chain reaction (RT-PCR) approach. Results The expression of bcl-2 mRNA in MCF-7 cells increased significantly after exposure to octylphenol and E 2 24 h and the effects continued to 120 h. The stimulation effect on the expression of bcl-2 mRNA was induced by octylphenol with a wide range of concentrations, and the strongest effect was found at the concentration of 10-6 mol/L of octylphenol. Conclusion The results suggested that octylphenol had similar estrogenic activities as E 2 on regulating the expression of bcl-2 mRNA in MCF-7 cells, but the effect was weaker than that of E 2.
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Objective To study the effect of bisphenol A (BPA) and dibutyphthlate (DBP) treated with Rat Liver S9 on proliferation MCF-7 cells. Methods Added the positive control 17?-estradiol (E2) and compounds of BPA and DBP with the effect of Rat Liver S9 to MCF-7 cells proliferation respectively and determinated the quantity of MCF-7 cells with MTT assay. Results The activity of E2 and DBP stimulated MCF-7 cells decreasing significantly with the effect of Liver S9 than without the effect of Liver S9, while BPA stimulated MCF-7 cells increasing significantly with the effect of Liver S9 than that without the effect of Liver S9. Conclusion E2 and DBP have a lower estrogenic activity with the effect of S9 than without the effect of S9. BPA shows a higher estrogenic activity with the effect of S9 than without the effect of S9.
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The effect of estradiol–17ß and progesterone given separately as well as in combination on the rate of hydrogen peroxide formation and lipid peroxidation in the uteri of ovariectomized rats was studied. Estradiol in 3 μg dose per day per animal elicited maximum stimulatory response and progesterone (100 μg), on the other hand, was without any such effect. However, progesterone given along with estradiol completely prevented the effect due to the latter. In the same way, vitamin E, a well known antioxidant was found to be extremelv effective in protecting the uterus from the highly peroxidative action of estradiol–17ß.
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Aim To observe the effects of 17?-estradiol(E2)and exercise on the protein expression of peroxisome proliferators activated receptor ?(PPAR?)in bone tissues and bone marrow adipocytes in ovariectomized rats.Methods Forty female Sprague-Dawley rats,aged three months,were randomly divided into the following four groups:sham-operation(Sham),ovariectomized(OVX),ovariectomized plus moderate-intensity treadmill exercise(EX,18 m?minute-1,45 min?day-1,5 uphill,4 times?week-1)and ovariectomized treated with E2(25 ?g?kg-1,3 times?week-1)group.At the end of experiment,the morphological changes of femur and tibia were observed decalcifiedly by HE staining and the protein expression of bone PPAR? was detected by Western blot.Results The number of fat vacuoles and PPAR? protein expression in OVX group was significantly higher than that of other three groups.Conclusion E2 and exercise can benefit the bone morphological structure and these effects might be partly related to the inhibition of both PPAR? protein expression in bone tissues and adipogenic differentiation of bone marrow in OVX rats.
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Objective To study the effect of 17?-estradial(E-2) on apoptosis of cardiomyocytes induced by norepinephrine(NE) in vitro and its mechanism. Methods The cultured neonatal rat cardiomyocytes were treated with NE(50??mol/L),E-2(10?nmol/L) or NE(50??mol/L)+E-2(10?nmol/L) respectively in serum-free DMEM for 48?h.The morphological changes of myocytes were studied by phase-microscopy and transmission electron microscopy;apoptosis was identified by DNA laddering and apoptotic rate was assayed by flow cytometer;cfos protein in cardiomyocytes was detected using semiquantitative immunofluorescence cytochemistry technique. Results 17?-estradiol inhibited the morphological changes of apoptotic cardiomyocytes induced by norepinephine such as cell atrophy,condensed chromatin clumps against the nuclear envelope associated with swelling of mitochondria and presentation of apoptotic body,DNA laddering disappeared,the apoptotic rate decreased and the expression of c-fos protein inhibited in cardiomyocytes.Conclusion 17?-estradiol can protect cultured cardiomyocytes from apoptosis induced by norepinephrine,its mechanism might associate with suppression of c-fos protein expression.
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Objective To observe effects of 17?-estradiol on phenylephrine-induced hypertrophy in cultured neonatal rat cardiomyocytes and to explore its mechanisms. Methods Using cultured neonatal rat cardiomyocytes treated with different factors as a model,surface area of cardiomyocytes was measured by computer photograph analysis software;the protein synthesis rate was assayed with leucine intake method;the proto-oncogene c-fos protein expression was assessed with immunocytochemistry technique;the markers of cardiomyocyte hypertrophy,embryonic genes such as ?-MHC\,?-skA and ANP mRNA expressions were assessed with semiquantitative reverse transcription-PCR. Results 17?-estradiol inhibited obviously phenylephrine-induced increase of surface area and the protein synthesis rate of cardiomyocytes,reduced c-fos protein expression of hypertrophic cardiomyocytes,and down-regulated ?-MHC、?-skA mRNA expressions and up-regulated ANP mRNA expression.Conclusion 17?-estradiol inhibits hypertrophy of cardiomyocytes and its mechanisms might be related with the suppression of c-fos protein expression,the reversion of the embryonic switching of contractile protein genes(?MHC and ?-skA),the increase of ANP mRNA expression.