OBJECTIVETo study 17β-estradiol (E2), ethinylestradiol (EE2), estriol (E3), estrone (E1) on MCF-7 proliferation effects, and compare the effects of independent action (IA) model with concentration addition (CA) model in assessing the combined effects of estrogen.

METHODSThe combinations of E2 + EE2, E2 + E3 and E2 + E1 were chosen and the cellular proliferation effects were examined by MTT assay.

RESULTSThe maximum proliferation effects at dose of 10⁻⁹ mol/L was 325.48% for E2, 330.34% for EE2, 255.22% for E3, and 199.61% for E1. In the E2 + EE2, E2 + E3, E2 + E1 groups, the results of IA model analysis were very close to the experimental results. The IA model tend to overestimated the experimental results, while the CA model often underestimated the experimental results. In the EC (E2, 30) + C (EE2, 70) group, the results exceed the maximum estrogen effects of E2, while in other groups, the results were lower.

CONCLUSIONSThe estrogenic effects of the four tested substances from high to low efficiency were that: EE2 > E2 > E3 > E1. The effect of IA model in predicting the combined effects of binary mixture was better than CA model. A small proportion of binary mixture showed synergy.

Cell Line, Tumor ; Cell Proliferation ; drug effects ; Estradiol ; pharmacology ; Estriol ; pharmacology ; Estrogens ; pharmacology ; Estrone ; pharmacology ; Ethinyl Estradiol ; pharmacology ; Female ; Humans

The favorable effects of estrogen on cardiovascular diseases can be explained by several mechanisms such as changes in serum lipid profiles and thrombogenecity. Estrogen also affects the vascular tone, but there has been no report in which the effect of estrogen was tested comprehensively for several vasoactive substances, especially after long-term administration. Two weeks after bilateral ovariectomy in 8-week old female Sprague-Dawley rats, placebo or 17 beta-estradiol (E2) pellets (0.5 mg; released over 3 weeks) were implanted subcutaneously. Two weeks after pellet implantation, organ chamber experiments were performed using aortae. Compared with control, E2-treated vessels showed impaired endothelium-dependent relaxation to acetylcholine. E2 enhanced the contraction to norepinephrine and U46619 and had no effect on endothelin-1-induced contraction. In contrast, the contraction to angiotensin (AT)-II was inhibited by E2. Northern blot analysis for AT1 receptor expression using cultured aortic smooth muscle cells showed no difference between control and E2-treated cells, suggesting that AT1 receptor downregulation is not the likely mechanism. These results suggest that E2 affects the vascular tone variably according to vasoactive substances.
Animal ; Estradiol/pharmacology* ; Female ; In Vitro ; Ovariectomy* ; Rats ; Rats, Sprague-Dawley ; Vasoconstrictor Agents/pharmacology* ; Vasodilator Agents/pharmacology* ; Vasomotor System/drug effects*

AIM AND METHODSTo further explore the functions of alveolar macrophage and their modulation mechanisms, the activity of lysozyme in rat alveolar macrophage assessed by electrophoresis was determined. The effects of androsterone and estradiol on lysozyme secretion and their mechanisms were also studied.

RESULTSThe results showed that androsterone and estradiol increased activity of lysozyme significantly (P < 0.01), indomethacin abolished those effects. This suggests that the insufficiency of sex hormones secretion as the retrogression of gonads is involved in the decrease of immunological functions, and the susceptibility to infectious diseases.

CONCLUSIONSex hormones increased activity of lysozyme, and those effects related to prostaglandin.

Androsterone ; pharmacology ; Animals ; Estradiol ; pharmacology ; Female ; Indomethacin ; pharmacology ; Macrophages, Alveolar ; drug effects ; enzymology ; secretion ; Male ; Muramidase ; metabolism ; Rats ; Rats, Wistar

OBJECTIVETo investigate the effects of 17beta-estradiol on the expression of alkaline phosphatase (ALP) and osteoprotegerin in human periodontal ligament cells.

METHODSHuman periodontal ligament cells (hPDLC) were obtained from periodontal tissue explants of teeth extracted for orthodontic treatment ALP activity was determined by PNPP, and OPG protein and corresponding mRNA levels were quantitatively detected by ELISA and RT-PCR RESULTS: ALP activity was significantly increased at 14 days and 21 days (P <0.05). 17beta-E2 of physiological concentration promoted secretion of OPG protein and expression of OPG mRNA (P <0.05). 17beta-E2 with high-dose showed no effect on OPG protein secretion and decrease OPG mRNA expression.

CONCLUSIONS17beta-E2 may have a positive impact on periodontium through promoting expression of ALP and OPG in hPDLC.

Alkaline Phosphatase ; metabolism ; Cells, Cultured ; Estradiol ; pharmacology ; Humans ; Osteoprotegerin ; metabolism ; Periodontal Ligament ; cytology ; drug effects ; metabolism

Animals ; Estradiol ; blood ; pharmacology ; Hepatocyte Growth Factor ; metabolism ; Liver Cirrhosis ; metabolism ; pathology ; Male ; Rats ; Rats, Wistar

To investigate the electrophysiological effects of 17β-estradiol on pacemaker cells in sinoatrial (SA) nodes of rabbits and the underlying mechanism, intracellular microelectrode technique was used to record action potential (AP) in SA node cells of rabbits. The results showed that: (1) 17β-estradiol (1, 10, 100 μmol/L) not only significantly decreased the amplitude of action potential (APA) and the maximal rate of depolarization (V(max)), but also decreased the velocity of diastolic (phase 4) depolarization (VDD) and rate of pacemaker firing (RPF) in a concentration-dependent manner. The AP duration at 50% repolarization (APD(50)) and at 90% repolarization (APD(90)) were prolonged. But the maximal diastolic potential (MDP) was not affected. (2) Pretreatment with tamoxifen (10 μmol/L), an inhibitor of estrogen receptor, did not block the electrophysiological effects of 17β-estradiol (10 μmol/L) on SA node cells. (3) Pretreatment with N(G)-nitro-L-arginine methyl ester (L-NAME, 100 μmol/L), a nitric oxide (NO) synthase inhibitor, completely abolished the electrophysiological effects of 17β-estradiol (10 μmol/L) on SA node cells. The results suggest that 17β-estradiol inhibits the electrophysiological activity of pacemaker cells in SA nodes of rabbits in a concentration-dependent manner possibly through a non-genomic mechanism related with NO.
Action Potentials ; Animals ; Electrophysiological Phenomena ; Estradiol ; pharmacology ; Myocytes, Cardiac ; drug effects ; Rabbits ; Sinoatrial Node ; cytology

OBJECTIVESTo confirm whether regeneration of prostate lobe indeed takes place on surgical lobectomy and if so, to what extent. Other issues studied are 1. whether the lobe regenerated is similar morphologically to that developing normally from neonatal origin to adulthood, and 2. the consequences of partial lobectomy on the contralateral lobe and the influence of sex steroid hormones on the regeneration process.

METHODSThe effect of surgical removal of one of the ventral prostate lobes on the size of the contralateral lobe has been studied at various time intervals after lobectomy.

RESULTSThe surgically extirpated ventral prostate lobe in rats regenerates attaining plateau size at 8-16 weeks post lobectomy. The regenerated lobe, however, remains significantly smaller than the original size. In early phase of post lobectomy (at 2 weeks) the contralateral lobe was significantly hypertrophied. It reverts to normal size on regeneration of the extirpated lobe with time. Orchiectomy carried out at the time of lobectomy caused a drastic reduction in the size of the remaining lobe, which was prevented by exogenous treatment with androgens. In animals receiving treatment with estrogens, the remaining lobe was partially but not fully atrophied. However, estrogens did not support the regeneration of the surgically removed lobe, which requires androgens.

CONCLUSIONSThese studies demonstrate that surgical removal of one of the ventral prostate lobe leads to a process of regeneration. However, the regenerated lobe does not attain the normal size.

Animals ; Estradiol ; pharmacology ; Male ; Orchiectomy ; Prostate ; drug effects ; physiology ; Prostatectomy ; Prostatic Hyperplasia ; etiology ; Rats ; Rats, Wistar ; Regeneration ; Testosterone ; pharmacology

Animals ; Cadherins ; metabolism ; Catenins ; metabolism ; Estradiol ; pharmacology ; Estrogen Receptor Modulators ; pharmacology ; Female ; Ovariectomy ; Rats ; Uterus ; drug effects ; metabolism

Amyloid beta-Peptides ; toxicity ; Animals ; Drugs, Chinese Herbal ; pharmacology ; Estradiol ; pharmacology ; PC12 Cells ; Peptide Fragments ; toxicity ; Rats

To investigate the relationship between the expression of cyclooxygenase-2 (COX-2) and menstrual cycle, the regulatory effects of 17-beta-estradiol (E(2)) and medroxyprogesterone acetate (MPA) on the expression of COX-2 in cervical cancer Hela cells were examined. Cervical cancer specimens were obtained from 47 pre-menopausal patients. The phase of menstrual cycle was determined by case history and HE staining of uterine endometrium. COX-2 was immunohistochemically stained by SABC staining and the staining intensity was determined with computerized image analysis system. Hela cells were incubated with alcohol, E(2), E(2)+MPA, MPA for 12, 24 and 48 h respectively. The expression of COX-2 in Hela cells was detected by Western blotting and reverse transcriptase-polymerase chain reaction (RT-PCR). Our results showed that the expression of COX-2 was significantly higher during proliferative phase than secretory phase (P<0.05), but there was no difference in the positive rate between proliferative phase and secretory phase (P>0.05). Incubation with E(2) could significantly enhance the expression of COX-2 continually. On the contrary, E(2)+MPA and MPA alone could decrease the expression of COX-2 as compared with the control and E(2) group (P<0.05 and P<0.01 respectively). It is concluded that the expression of COX-2 in cervical cancer of pre-menopausal patients and Hela cells was regulated by estrogen/progestogen.
Cyclooxygenase 2/genetics ; Cyclooxygenase 2/*metabolism ; Estradiol/*pharmacology ; Hela Cells ; Medroxyprogesterone Acetate/*pharmacology ; Uterine Cervical Neoplasms/*enzymology