J Bone Miner Res. 2002 Apr;17(4):630-8.
Down-regulation of osteoclast differentiation by daidzein via caspase 3.
Rassi CM, Lieberherr M, Chaumaz G, Pointillart A, Cournot G.
CNRS UPR 1524, Jouy en Josas, France.
Phytoestrogens are plant-derived compounds with estrogen-like activity. Phytoestrogen-rich diets may prevent postmenopausal osteoporosis and these molecules maintain bone mass in ovariectomized animals. We compared the effects of the isoflavone daidzein, which has no action on tyrosine kinases, and 17beta-estradiol on the development and activity of osteoclasts in vitro. Nonadherent porcine bone marrow cells were cultured on dentine slices or on culture slides in the presence of 10-8 M of 1,25-dihydroxyvitamin D3 [1,25(OH)2D3], with or without 10(-8) M of daidzein, 10(-8) M of 17beta-estradiol for 9-11 days. Multinucleated tartrate-resistant acid phosphatase-positive (TRAP+) cells that resorbed bone (osteoclasts) developed in the presence of 1,25(OH)2D3. The number of osteoclasts formed in response to 1,25(OH)2D3 was reduced by 58 +/- 8% by daidzein and 52 +/- 5% by estrogen (p < 0.01); these effects were reversed by 10-6 M of ICI 182,780. The area resorbed by mature osteoclasts was reduced by 39 +/- 5% by daidzein and 42 +/- 6% by estradiol (p < 0.01). Both compounds also inhibited the 1,25(OH)2D3-induced differentiation of osteoclast progenitors (mononucleated TRAP+ cells), 53 +/- 8% by daidzein and 50 +/- 7% by estradiol (p < 0.05). Moreover, daidzein and estradiol promoted caspase-8 and caspase-3 cleavage and DNA fragmentation of monocytic bone marrow cells. Caspase-3 cleavage was reversed by 10-8 M of ICI 182,780. Both compounds up-regulated the expression of nuclear estrogen receptors ER-alpha and ER-beta. Thus, daidzein, at the same concentration as 17beta-estradiol, inhibits osteoclast differentiation and activity. This may be caused by, at least in part, greater apoptosis of osteoclast progenitors mediated by ERs.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11918220&dopt=Abstract estradiol [PubMed - indexed for MEDLINE
Acta Pharmacol Sin. 2002 Mar;23(3):273-7.
Inhibition of beta-estradiol on trachea smooth muscle contraction in vitro and in vivo.
Pang JJ, Xu XB, Li HF, Zhang XY, Zheng TZ, Qu SY.
Department of Physiology, Lanzhou Medical College, Lanzhou 730000, China.
AIM: To investigate the effect of beta-estradiol on trachea smooth muscle contraction in vitro and in vivo. METHODS: (1) Rabbit tracheas were incubated in organ baths filled with Krebs solution and supplied with a mixed gas of 95 % O2 and 5 % CO2. The isometric force was measured by ink-writing recorders. (2) The incubation period of asthma induced by histamine and acetylcholine (ACh) in guinea pig were measured before and after beta-estradiol (1 mg/kg) were given intramuscularly. RESULTS: (1) Administration of beta-estradiol (0.1 mmol/L) caused relaxation of isolated trachea muscle strips (TMS) in rabbits pre-contracted by ACh and KCl (39 % +/- 5 % and 45 % +/- 19 %). The presence of indomethacin or methylene blue partly decreased the relaxation to beta-estradiol (26 % +/- 8 % and 28 % +/- 13 %), but Nomega-nitro-L-arginine (L-NNA) and propranolol and epithelium removal did not affect it (38 % +/- 10 %, 40 % +/- 15 %, 37 % +/- 8 %). beta-Estradiol can shifted the concentration-response curves of ACh and CaCl2 to the rightward (pD2 = 3.98 and 4.75). In addition, it could also significantly inhibit the contraction of phase caused by ACh, but did not affect the contraction of phase II caused by CaCl2. (2) The incubation period of asthma in guinea pig were delayed by beta-estradiol (1 mg/kg) given intramuscularly. CONCLUSION: (1) The relaxation of beta-estradiol in vitro was epithelium independent and associated with the inhibition of potential-dependent channel and release of Ca2+ from sarcoplasm reticulum induced by ACh. In addition, release of prostaglandins from trachea smooth muscle cells and relaxation through cGMP approach were also included. beta-Adrenoceptor-mediated relaxation was not involved. (2) beta-Estradiol can relax the trachea i
J Bone Miner Res. 2002 Apr;17(4):593-602.
Human osteoblasts' proliferative responses to strain and 17beta-estradiol are mediated by the estrogen receptor and the receptor for insulin-like growth factor I.
Cheng MZ, Rawlinson SC, Pitsillides AA, Zaman G, Mohan S, Baylink DJ, Lanyon LE.
The Royal Veterinary College, University of London, United Kingdom.
The mechanism by which mechanical strain and estrogen stimulate bone cell proliferation was investigated using monolayer cultures of human osteoblastic TE85 cells and female human primary (first-passage) osteoblasts (fHOBs). Both cell types showed small but statistically significant dose-dependent increases in [3H]thymidine incorporation in response to 17beta-estradiol and to a single 10-minute period of uniaxial cyclic strain (1 Hz). In both cell types, the peak response to 17beta-estradiol occurred at 10(-8) - 10(-7) M and the peak response to strain occurred at 3500 microstrain ((mu)epsilon). Both strain-related and 17beta-estradiol-related increases in [3H]thymidine incorporation were abolished by the estrogen receptor (ER) modulator ICI 182,780 (10-8 M). Tamoxifen (10(-9) - 10(-8) M) increased [3H]thymidine incorporation in both cell types but had no effect on their response to strain. In TE85 cells, tamoxifen reduced the increase in [3H]thymidine incorporation associated with 17beta-estradiol to that of tamoxifen alone but had no such effect in fHOBs. In TE85 cells, strain increased medium concentrations of insulin-like growth factor (IGF) II but not IGF-I, whereas 17beta-estradiol increased medium concentrations of IGF-I but not IGF-II. Neutralizing monoclonal antibody (MNAb) to IGF-I (3 microg/ml) blocked the effects of 17beta-estradiol and exogenous truncated IGF-I (tIGF-I; 50 ng/ml) but not those of strain or tIGF-II (50 ng/ml). Neutralizing antibody to IGF-II (3 microg/ml) blocked the effects of strain and tIGF-II but not those of 17beta-estradiol or tIGF-I. MAb aIR-3 (100 ng/ml) to the IGF-I receptor blocked the effects on [3H]thymid
World J Gastroenterol. 2002 Apr;8(2):363-6.
Protective effect of estradiol on hepatocytic oxidative damage.
Liu Y, Shimizu I, Omoya T, Ito S, Gu XS, Zuo J.
Department of Biology, Medical School of Fudan University, 130 Dongan Road, Shanghai 210032, China. liya989ahoo.com
AIM: To examine the protective effect of estradiol on the cultured hepatocytes under oxidative stress. METHODS: Hepatocytes of rat were isolated by using perfusion method, and oxidative stress was induced by a serum-free medium and FeNTA. MDA level was determined with TBA method. Cell damage was assessed by LDH assay. Apoptosis of hepatocytes was assessed with cytoflowmetric analysis. Expression of Bcl-xl in cultured hepatocytes was detected by Western blot. The radical-scavenging activity of estradiol was valued by its ability to scavenge the stable free radical of DDPH. RESULTS: Oxidative stress increased LDH from 168 +/- 25 x 10(-6)IU.cell(-1) to 780 +/- 62 x 10(-6)IU.cell(-1) and MDA(from 0.28 +/- 0.07 x 10(-6)nmol.cell(-1) to 1.35 +/- 0.12 x 10(-6)nmol.cell(-1)) levels in cultured hepatocyte, and estradiol inhibited both LDH and MDA production in a dose dependent manner. In the presence of estradiol 10(-6)mol.L(-1), 10( -7 )mol.L(-1) and 10(-8)mol.L(-1),the LDH levels are 410 +/- 53 x 10(-6)IU.cell(-1) (P<0.01 vs oxidative group), 530 +/- 37 X 10(-6)IU.cell(-1 ) (P<0.01 vs oxidative group), 687+/-42 x 10(-6)IU.cell(-1) (P<0.05 vs oxidative group) respectively, and the MDA level are 0.71+/-0.12 x 10(-6)nmol.cell(-1) (P<0.01 vs oxidative group),0.97+/-0.11 x 10(-6)nmol.cell(-1 )(P<0.01 vs oxidative group) and 1.27+/-0.19 x 10(-6)nmol.cell(-1) respectively. Estradiol suppressed apoptosis of hepatocytes induced by oxidative stress, administration of estradiol(10(-6)mol/L)decreased the apoptotic rate of hepatocytes under oxidative stress from 18.6 +/- 1.2% to 6.5 +/-2.5%, P<0.01. Bcl-xl expression was related to the degree of liver cell damage due to oxidative stress, and estradiol showed a protective actio
Biochem Pharmacol. 2002 Mar 15;63(6):1177-81.
The effects of natural ligands of hormone receptors and their antagonists on telomerase activity in the androgen sensitive prostatic cancer cell line LNCaP.
Bouchal J, Kolar Z, Mad'arova J, Hlobilkova A, von Angerer E.
Laboratory of Molecular Pathology, CMBM and Institute of Pathology, Faculty of Medicine, Palacky University, Olomouc, Czech Republic.
The effects of the 17beta-estradiol, dihydrotestosterone and hormone antagonists tamoxifen and bicalutamide on telomerase activity and expression of cell cycle related proteins in the androgen-sensitive prostatic cancer cell line LNCaP were studied. The cell line was grown in RPMI supplemented with 2.5% charcoal-stripped FBS for 72 hr. The IC(50) of tamoxifen and bicalutamide and the optimal stimulatory concentrations of 17beta-estradiol and dihydrotestosterone were determined by means of the cell-viability assay, the activity of telomerase was measured by the telomere repeat amplification protocol (TRAP) and the expression of proteins was analysed by the Western blot technique. 17beta-estradiol stimulated cell growth more effectively than dihydrotestosterone whereas hormone antagonists tamoxifen and bicalutamide caused a significant decrease in cell viability. The treatment of cells by a combination of low doses of 17 beta-estradiol and dihydrotestosterone stimulated cells stronger than treatment by a single hormone. Only 17beta-estradiol, in concentration of 10nM, increased strongly the expression of p21(Waf1/Cip1) and increased slightly telomerase activity in the LNCaP cells. 50 microM of bicalutamide down-regulated the levels of the androgen receptor, the proliferating cell nuclear antigen and telomerase activity, and up-regulated the expression of p27(Kip1). We hereby describe the first observation of the influence of bicalutamide on telomerase activity and a positive correlation between the effect of 17beta-estradiol and the induction of both the endogenous cyclin-dependent kinase inhibitor, p21(Waf
Anal Bioanal Chem. 2002 Jan;372(2):293-300. Epub 2001 Dec 18.
Characterisation of antibodies and analytes by surface plasmon resonance for the optimisation of a competitive immunoassay based on energy transfer.
Coille I, Gauglitz G, Hoebeke J.
Institut of Physical and Theoretical Chemistry, University of Tubingen, Germany.
The determination of binding constants using surface plasmon resonance (SPR) was introduced to optimise a competitive homogeneous fluorescence energy-transfer immunoassay (ETIA) before labelling. Steroids were chosen as model for the detection of three analytes estrone, estradiol and ethinylestradiol--by taking three polyclonal antibodies (anti estrone-, anti estradiol- and anti estrogen-antibodies) and the corresponding analyte derivatives used for the immunisation. The active concentration of the antibodies was determined before and after labelling. Inhibition curves were recorded using SPR for all possible combinations of analyte, antibody, and analyte derivatives. The experiments revealed that the active antibody concentration can be reduced to 30% whereas the antibody affinity is not affected by the labelling process. Limits of the use of SPR for determination of affinity constants in solution are discussed. All possible ETIA calibration for the quantification of estrone and estradiol was performed. The lower limits of detection for estrone (0.06 microg L(-1)) and estradiol (0.17 microg L(-1)) were reached with the anti-estrogen IgG and its derivative
Environ Toxicol Chem. 2003 Apr;22(4):866-71.
Induction of an estrogen-responsive reporter gene in rainbow trout hepatoma cells (RTH 149) at 11 or 18 degrees C.
Hornung MW, Ankley GT, Schmieder PK.
US Environmental Protection Agency, Office of Research and Development, National Health and Environmental Effects Research Laboratory, Mid-Continent Ecology Division, 6201 Congdon Boulevard, Duluth, Minnesota 55804, USA. hornung.michaepa.gov
The potential for temperature to influence estrogen-mediated responses in poikilothermic animals suggested that temperature may be an important variable to consider when using an estrogen-responsive reporter gene in a rainbow trout cell line to test chemicals for estrogenic activity. Rainbow trout hepatoma cells (RTH 149) incubated at 11 or 18 degrees C were cotransfected with an estrogen-responsive luciferase reporter plasmid and a plasmid containing a constitutively expressed rainbow trout estrogen receptor. The RTH-149 cells were then exposed to estradiol, with samples collected at 24-h intervals. The 72-h effective concentration for 50% maximal response (EC50) for estrogen-responsive luciferase activity at 11 degrees C was 3.8 x 10(-9) M and 7.4 x 10(-10) M at 18 degrees C. The efficacy of estradiol was lower at 11 degrees C. The maximal response to estradiol in cells at 11 degrees C was generally two- to threefold greater than controls (mean = 2.6-fold), whereas the maximal response at 18 degrees C was three- to fourfold greater than controls (mean = 3.2-fold). Ethinylestradiol, a strong estrogen receptor agonist, was similar to estradiol in potency (relative potency = 0.8) and efficacy at the two temperatures. The EC50 of the weak estrogen receptor agonist 4-tert-pentylphenol was 7.6 x 10(-7) M at 11 degrees C and 6.9 x 10(-7) M at 18 degrees C; its potency relative to 17beta-estradiol was not significantly different at the two temperatures, 0.00036 and 0.00054 at 11 degrees C and 18 degrees C, respectively. The estrogen-responsive reporter gene activity p
Wei Sheng Yan Jiu. 1998 Nov 30;27(6):396-9.
[Kinetic effect of testosterone or estradiol on iodine absorption in castrating rat intestine]
[Article in Chinese]
Wu N, Ye G, Tang Z.
Institute of Child and Adolescent Health, Beijing Medical University, Beijing 100083, China.
OBJECTIVE: To observe the effect of testosterone or estradiol on iodine absorption in rat intestine. METHOD: 50 male adult Wistar rats were divided into 5 groups randomly. 50 females were divided into another 5 groups. Among them, 4 groups were bilaterally testectomized or ovariectomized, 1 group was sham-operated. 7 days after operation, the castrated rats received testosterone (male rats) or estradiol (female rats) at different dosages by intramuscular injection for three days. Then the kinetics of iodine absorption in jejunum and ileum were observed by perfusion in situ. When finished, serum were obtained for detecting TSH, T4 and testosterone or estradiol. RESULTS: In castrated male rats, the value of K12 reduced, K21 increased, K02 reduced, and SP1/2 (the half time of the slow phase) prolonged, implying that the ability of iodine absorption reduced. It reflected that testosterone could promote iodine absorption in intestine in physiological condition. In castrated female rats, the situation was different from that in male rats, the value of K12 increased, K21 reduced, K02 increased, and SP1/2 shortened in jejunum, implying that the ability of iodine absorption increased. It reflected that estradiol could inhibit iodine absorption in intestine in physiological condition. The levels of serum TSH and T4 were not changed significantly in this experiment. CONCLUSION: In physiological condition, testosterone can promote iodine absorption, while estradiol has the inhibiting effect. The results indicate that gonadol hormone maybe one factor which can influence iodine absorption in intestine. It may explain the phenomenon that the incidence of goiter is different between males and females partly.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11939028&dopt=Abstract estradiol [PubM
Sheng Li Xue Bao. 2000 Dec;52(6):515-8.
[Modulatory effects of 17beta-estradiol on the electrical activity of subfornical organ neurons]
[Article in Chinese]
Wang H, Wang ZA, He RR.
Department of Physiology, Institute of Basic Medicine, Hebei Medical University, Shijiazhuang 050017, China.
The effects of 17beta-estradiol (E(2) ) on electrical activity of neurons in subfornical organ (SFO) slices were examined using extracelluar recording technique. The results are as follows. (1) In 15 SFO units, a low dose of E(2) (0.1 nmol/L) applied into superfusate induced an increase in discharge rate from 3.21+/-0.37 to 6.79+/-0.71 Hz (P<0.001), whereas a high dose of E(2) (100 nmol/L ) caused a decrease in discharge rate from 3.44+/-0.40 to 1.44+/-0.36 Hz (P<0.01); (2) glutamate NMDA receptor antagonist MK-801 (50 pmol/L) blocked the excitatory effects induced by low dose of 17beta-estradiol in 7 units; (3) L-arginine (L-arg, 1 mmol/L), a physiological precursor of NO, abolished the excitatory effects induced by low dose of 17beta-estradiol in 7 units; (4) application of N-omega-nitro-L-arginine methyl ester (L-NAME, 10 mmol/L), an inhibitor of NOS, blocked the inhibitory effects induced by high dose of 17beta-estradiol in 6 units. The above results suggest that the estrogen exerts dual action on SFO neuron. E(2) at low dosage increases the discharge rate of SFO neuron, an effect which may be related to the activation of NMDA receptors, whereas E(2) at high dosage decreases the discharge rate, an effect which may be attributed to the activation of NOS with resultant production of NO.
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