scholarly journals Mongolian Medicine RuXian-I Treatment of Estrogen-Induced Mammary Gland Hyperplasia in Rats Related to TCTP Regulating Apoptosis

2019 ◽  
Vol 2019 ◽  
pp. 1-10 ◽  
Author(s):  
Jun-Fei Zhang ◽  
Jia Liu ◽  
Guo-Hua Gong ◽  
Bin Zhang ◽  
Cheng-Xi Wei
Keyword(s):  
Mammary Gland ◽  
Breast Tissue ◽  
Caspase 3 ◽  
Mammary Glands ◽  
The Body ◽  
Therapeutic Activity ◽  
Pathological Changes ◽  
Caspase 9 ◽  
Organ Index ◽  
Therapeutic Mechanism

Mongolian medicine RuXian-I is composed of 30 Mongolian herbs, which is a traditional Mongolian recipe for clinical treatment of breast “Qi Su Bu Ri Le Du Sen” disease (hyperplasia of mammary glands, HMG). Based on the previous study, this dissertation further explores the therapeutic mechanism of RuXian-I on estrogen-induced HMG in rats. RuXian-I had no effect on the body weight and food intake of HMG rats and had no toxic effects on the five organs (heart, lung, spleen, and kidney). RuXian-I reduced the diameter and height of nipple, organ index, and pathological changes and alleviated the sex hormone levels oh HMG; RuXian-I reduced the upregulation of TCTP, Mcl-1, and Bcl-xL in breast tissue of mammary gland hyperplasia and increased the downregulation of p53, Bax, caspase-9, and caspase-3 protein. RuXian-I has an effective therapeutic activity on HMG rats, and its possible therapeutic mechanism is closely related to antiapoptosis protein TCTP-regulated apoptosis.

scholarly journals Reversible physiological transdifferentiation in the adipose organ

2009 ◽  
Vol 68 (4) ◽  
pp. 340-349 ◽  
Author(s):  
Saverio Cinti
Keyword(s):  
Mammary Gland ◽  
Cell Biology ◽  
Mammary Glands ◽  
The Body ◽  
Lactation Period ◽  
Brown Adipocytes ◽  
White Adipocytes ◽  
Hormonal Stimulus ◽  
Adipose Organ ◽  
Adipose Cells

All mammals are provided with two distinct adipose cells, white and brown adipocytes. White adipocytes store lipids to provide fuel to the organism, allowing intervals between meals. Brown adipocytes use lipids to produce heat. Previous descriptions have implied their localization in distinct sites of the body; however, it has been demonstrated that they are present together in many depots, which has led to the new concept of the adipose organ. In order to explain their coexistence the hypothesis of reversible physiological transdifferentiation has been developed, i.e. they are contained together because they are able to convert, one into the other. In effect, if needed the brown component of the organ could increase at the expense of the white component and vice versa. This plasticity is important because the brown phenotype of the organ is associated with resistance to obesity and its related disorders. A new example of reversible physiological transdifferentiation of adipocytes is offered by the mammary gland during pregnancy, lactation and post-lactation stages. The gravidic hormonal stimulus seems to trigger a transdifferentiation of adipocytes into milk-producing and secreting epithelial glands. In the post-lactation period some of the epithelial cells of the mammary gland seem to transdifferentiate into adipocytes. Recent unpublished results suggest that explanted adipose tissue, as well as explanted isolated mature adipocytes, is able to transdifferentiate into glands with epithelial markers of milk-secreting mammary glands. These findings, if confirmed, seem to suggest new windows into the cell biology frontiers of adipocytes.

INTERACTIONS OF OESTROGENS AND ANDROGENS ON THE MAMMARY GLAND AND GROWTH OF OTHER TISSUES IN HYPOPHYSECTOMIZED RATS TREATED WITH INSULIN, CORTISONE AND THYROXINE

1962 ◽  
Vol 41 (2) ◽  
pp. 287-300 ◽  
Author(s):  
Dora Jacobsohn
Keyword(s):  
Mammary Gland ◽  
Mammary Glands ◽  
The Body ◽  
List Type ◽  
Simultaneous Treatment ◽  
Abnormal Response ◽  
Hypophysectomized Rats ◽  
Different Doses

ABSTRACT In a previous study it was found that oestrogens are necessary for androgens to elicit a development of alveolar lobules in the mammary glands of rats. Since androgens and oestrogens exert synergistic as well as antagonistic actions on mammary glands of e. g. rabbits, the significance of oestrogens in the response of the mammary gland to androgens was further investigated in the rat. The experiments were designed according to the same principles as previously, that is, the response of the gland itself to oestrogens was modified. This was achieved by treatment of hypophysectomized rats with a) thyroxine (negligible response) and b) thyroxine, cortisone and insulin (marked response). The effect of endogenous androgens was studied in males injected with PMS with or without oestrogens. Gonadectomized rats were injected with testosterone and oestrogens. No oestrogens given: The mammary glands of hypophysectomized males injected with PMS showed an abnormal response, irrespective of simultaneous treatment with thyroxine, cortisone and insulin in various combinations. The result confirms previous work with testosterone. Negligible response of the mammary glands to oestrogens: In hypophysectomized rats treated with thyroxine, oestrogens and PMS or testosterone, the response of the glands was uniform and abnormal. The absence of end buds indicated that the response to oestrogens, if present at all, was suppressed by the androgens. Marked response of the mammary glands to oestrogens: In hypophysectomized rats treated with thyroxine, cortisone and insulin another response of the glands to androgens and oestrogens was found. Besides abnormal structures, alveolar lobules were present. The changes produced with different doses of testosterone and oestrone indicated a complicated interplay of the two hormones. Confirming previous observations, records of the length and weight of the body and of the weight of the liver and heart revealed marked growth in the hypophysectomized rats treated with thyroxine, cortisone and insulin.

scholarly journals Insulin-like growth factor binding protein-5 (IGFBP-5) induces premature cell death in the mammary glands of transgenic mice

Development ◽  
2002 ◽  
Vol 129 (19) ◽  
pp. 4547-4557 ◽  
Author(s):  
Elizabeth Tonner ◽  
Michael C. Barber ◽  
Gordon J. Allan ◽  
James Beattie ◽  
John Webster ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Cell Death ◽  
Mammary Gland ◽  
Transgenic Mice ◽  
Dna Content ◽  
Caspase 3 ◽  
Transgenic Animals ◽  
Mammary Glands ◽  
Mammary Development ◽  
Igf I

We have previously demonstrated that IGFBP-5 production by mammary epithelial cells increases dramatically during involution of the mammary gland. To demonstrate a causal relationship between IGFBP-5 and cell death we created transgenic mice expressing IGFBP-5 in the mammary gland using a mammary-specific promoter, β-lactoglobulin. DNA content in the mammary glands of transgenic mice was decreased as early as day 10 of pregnancy. Histological analysis indicated reduced numbers of alveolar end buds, with decreased ductal branching. Transgenic dams produced IGFBP-5 in their milk at concentrations similar to those achieved at the end of normal lactation. Mammary cell number and milk synthesis were both decreased by approximately 50% during the first 10 days of lactation. BrdU labelling was decreased, whereas DNA ladders were increased in transgenic animals on day 1 of lactation. On day 2 postpartum, the epithelial invasion of the mammary fat pad was clearly impaired in transgenic animals. The concentrations of the pro-apoptotic molecule caspase-3 and of plasmin were both increased in transgenic animals whilst the concentrations of 2 prosurvival molecules Bcl-2 and Bcl-xLwere both decreased. In order to examine whether IGFBP-5 acts by inhibiting the survival effect of IGF-I we examined IGF receptor phosphorylation and Akt phosphorylation and showed that both were inhibited. We attempted to “rescue” the transgenic phenotype by using growth hormone to increase endogenous IGF-I concentrations or by implanting minipumps delivering an IGF-1 analogue, R3-IGF-1, which binds weakly to IGFBP-5. Growth hormone treatment failed to affect mammary development suggesting that increased concentrations of endogenous IGF-1 are insufficient to overcome the high concentrations of IGFBP-5 produced by these transgenic animals. In contrast mammary development (gland weight and DNA content) was normalised by R3-IGF-I although milk production was only partially restored. This is the first demonstration that over-expression of IGFBP-5 can lead to; impaired mammary development, increased expression of the pro-apoptotic molecule caspase-3, increased plasmin generation and decreased expression of pro-survival molecules of the Bcl-2 family. It clearly demonstrates that IGF-I is an important developmental/survival factor for the mammary gland and, furthermore, this cell death programme may be utilised in a wide variety of tissues.

THE EFFECT OF CORTISOL ACETATE ON OESTRONE-INDUCED MAMMARY GLAND GROWTH IN IMMATURE OVARIECTOMIZED ALBINO MICE

1957 ◽  
Vol 16 (1) ◽  
pp. 72-79 ◽  
Author(s):  
R. E. MUNFORD
Keyword(s):  
Mammary Gland ◽  
Unit Area ◽  
Mammary Glands ◽  
Mammary Development ◽  
The Body ◽  
Logarithmic Scale ◽  
Uterine Weight ◽  
Gland Weight ◽  
Ovariectomized Mice ◽  
Albino Mice

SUMMARY The response of the mammary glands of ovariectomized albino mice to treatment with 0·003 or 0·006 μg oestrone daily could be distinguished after 21 days of treatment. Differences in mammary gland areas of oestrone-treated ovariectomized mice, and of both ovariectomized and intact controls, were significant. When injected at a level of 12·5 μg daily for 21 days, cortisol acetate (CA) stimulated mammary development in ovariectomized and ovariectomized oestrone-treated albino mice, both growth in area and increase in the number of duct junctions being affected. At higher dosage rates (25 and 50 μg daily) CA was without detectable influence on the mammary glands. The effect of the two steroids upon the mammary glands appeared to be simply additive when analysed on the transformed (logarithmic) scale. The estimate of the density of duct branching—number of duct junctions per unit area—of the mammary glands was not significantly affected by either steroid. Differences in this estimate of mammary gland structure were in general inversely related to differences in area or number of duct junctions. The effects of treatment with CA and with oestrone upon the body weight, adrenal and thymus gland weight, uterine weight and vaginal changes were also observed.

Mammary gland growth in relation to hormones with metabolic actions

1958 ◽  
Vol 149 (936) ◽  
pp. 325-329 ◽  
Keyword(s):  
Mammary Gland ◽  
Ovarian Hormones ◽  
Mammary Glands ◽  
Reproductive Organs ◽  
Growth Patterns ◽  
The Body ◽  
Sexual Cycle ◽  
Dense System ◽  
Biological Interest ◽  
High Doses

The mammary glands are poorly developed before puberty and consist at this period of a few short ducts. With approaching maturity the number and length of the ducts increases and, in females, alveoli can make their first appearance according to the type of sexual cycle. In many species the mammary glands develop a dense system of ducts and alveoli only during pregnancy, that is, shortly before the organ is becoming functionally active and producing milk. The amount and type of tissue constituting the mammary glands varies in different species. It often differs in members of the same species, sex and stage of sexual development. Apparently, the mammary gland reflects readily a variety of bodily changes in the growth patterns of its tissues. The study of this organ is of general biological interest not only because of the gland’s importance for the production of milk, but also as indicator of changes occurring in the internal environment of the body. The growth of the mammary glands is regulated by hormones. When the pituitary gland is present, ovarian hormones stimulate mammary gland growth in females and, in many species, also in males. In general, oestrogens elicit growth of ducts. Administration of progesterone together with oestrogens or alone in high doses results in a development of alveoli. The degree and type of growth depend upon the amounts available of both ovarian hormones. These facts seem to indicate that mammary gland growth is regulated in about the same manner as that of other reproductive organs, for instance the vagina and uterus.

scholarly journals Experience in treating breast pathology in outpatient practice

2020 ◽  
pp. 95-102
Author(s):  
M. Yu. Myasnyankin ◽  
V. V. Anisimov
Keyword(s):  
Staphylococcus Aureus ◽  
Mammary Gland ◽  
Breast Disease ◽  
Mammary Glands ◽  
The Body ◽  
Evidence Based ◽  
Adequate Treatment ◽  
Bacteriological Study ◽  
Fibrocystic Breast Disease ◽  
Starting Point

Introduction. According to epidemiological researches, such mammary gland disease as fibrocystic breast disease takes the leading place in the structure of pre-tumor diseases in women. Pathological cell proliferation is the common starting point for pathogenesis of both mastopathy and breast cancer. Patients with fibrocystic breast disease complain of pain unrelated to the menstrual cycle in the area of the mammary glands, swelling of breast tissue, nipple discharge. An important problem is the effective treatment of mastitis and lactostasis, during and after which the possibility of breastfeeding was maintained. Mastitis is a formidable complication of the postpartum period and the cause of lactation failure. For a long time, all patients with infectious mastitis underwent surgical treatment of the area of infection with subsequent drainage. As a rule, with the prescription of broad spectrum antibiotic drugs. Often, against the background of such stress for the body the ability to breastfeed dies down. Timely diagnosis and adequate treatment of mastitis and lactostasis help to preserve breastfeeding and improve the health of mother and child. Treatment of mastitis and lactostasis, fibrocystic breast disease is a complex problem of modern mammology.Aim. This paper presents a pathogenetic approach to the treatment of fibrocystic breast disease from the point of view of evidence-based medicine using micronized progesterone. In order to avoid surgical interventions on the mammary glands and to preserve the maximum possible period of breastfeeding, we studied and proposed the method of mini-invasive and evidence-based approach to the treatment and prophylaxis of mastitis and lactostasis using a drug containing the strain L. Fermentum CECT5716.Materials and methods. 13 patients with mastitis symptoms were included in the study. The main complaint of all patients who applied was lactostasis (100%). According to breast ultrasound, most patients were diagnosed with infiltrative mastitis – 8 (61.5%), serous mastitis – 4 (30.7%). Only one patient was diagnosed with purulent mastitis (7.7%). After prescription of treatment for mastitis and lactostasis after 21 days of clinical and radiological mammary gland image in 10 cases (77%) without pathology, duct ectasia was found in three women, which is the physiological norm in breastfeeding. All breastfeeding women have recovered normal lactation without symptoms of lactostasis. Almost all patients according to pain VAS noted not exceeding 1 point (mean was 1 ± 0.7). In most cases, the punctate cytogram corresponded to acute inflammation and purulent inflammation, 7 (53.9%) and 6 (46.1%). Results of a bacteriological study: Staphylococcus aureus – 11 (84.6%). Three patients had mixed microflora, Staphylococcus aureus/Staphylococcus epidermidis and Staphylococcus aureus/Staphylococcus saprophyticus, 2 (15.3%) and 1 (7.7%), respectively. One patient was diagnosed with Enterococcus faecalis. These data affected the choice of therapy. All patients were prescribed therapy with a drug containing the strain of L. Fermentum CECT5716 one capsule per day for 28 days, with subsequent assessment of the therapeutic effect on the 10th, 21st days.Results. After treatment on the 10th day of control examination all the patients had galactorrhea cytogram without morphological signs of inflammation. According to the data of the bacteriological study of cultures, complete elimination of pathogenic microflora was revealed in most cases – 8 (61,5%), in 5 patients there were titers of less than 104 CFU/ml, which was the norm indicator. Clinical examples of treatment are given.Conclusions. Our experience in treating such patients with a drug containing the strain L. Fermentum CECT5716 can successfully replace the standard of medical care for the treatment of mastitis and lactostasis. However, a combination with antibiotic therapy can be used for high bacterial load and mixed microflora. In all cases (100%) on the 10th day after the start of therapy all symptoms and clinical and radiological signs of lactostasis and mastitis were cured.

The effect of bromocriptine on mammary-gland ultrastructure of hyperprolactinemic rats

1984 ◽  
Vol 42 ◽  
pp. 204-205
Author(s):  
I.C. Murray
Keyword(s):  
Mammary Gland ◽  
Dopamine Agonist ◽  
Alveolar Epithelium ◽  
Mammary Glands ◽  
Female Rats ◽  
Control Group ◽  
Cell Hyperplasia ◽  
Once Daily ◽  
Long Evans

In women, hyperprolactinemia is often due to a prolactin (PRL)-secreting adenoma or PRL cell hyperplasia. RRL excess stimulates the mammary glands and causes proliferation of the alveolar epithelium. Bromocriptine, a dopamine agonist, inhibits PRL secretion and is given to women to treat nonpuerperal galactorrhea. Old female rats have been reported to have PRL cell hyperplasia or adenoma leading to PRL hypersecretion and breast stimulation. Herein, we describe the effect of bromocriptine and consequently the reduction in serum PRL levels on the ultrastructure of rat mammary glands.Female Long-Evans rats, 23 months of age, were divided into control and bromocriptine-treated groups. The control animals were injected subcutaneously once daily with a 10% ethanol vehicle and were later divided into a normoprolactinemic control group with serum PRL levels under 30 ng/ml and a hyperprolactinemic control group with serum PRL levels above 30 ng/ml.

INTERACTIONS OF OESTRONE AND TESTOSTERONE ON MAMMARY GLANDS OF MALE RABBITS

1961 ◽  
Vol 36 (1) ◽  
pp. 141-156 ◽  
Author(s):  
B. Bengtsson ◽  
A. Norgren
Keyword(s):  
Mammary Gland ◽  
Testosterone Propionate ◽  
Mammary Glands ◽  
List Type ◽  
Stunted Growth ◽  
Abnormal Growth ◽  
Growth Reaction ◽  
Extensive Growth ◽  
Higher Doses

ABSTRACT The effect of testosterone and oestrone on the mammary glands of castrated male rabbits was studied. Testosterone propionate was used in daily doses from 0.5 to 80 mg. The doses of oestrone ranged from 0.05 to 25 μg per day. Mammary glands were examined after 14, 28 or 56 days of injections. 1) Testosterone in doses below 20 mg failed to affect the mammary glands. With 40 or 80 mg a distinct, though abnormal growth reaction was consistently obtained. 2) Oestrone in doses lower than 0.5 μg did not stimulate mammary growth. With 0.5 μg and higher doses extensive growth of the mammary glands occurred. Stunted growth and secretion were found in the mammary glands of rabbits injected with 12.5 or 25 μg oestrone. 3) Testosterone in doses of 1 or 5 to 10 mg depressed or abolished the response of the mammary glands to 0.5 μg oestrone. When testosterone, in doses ineffective when given alone, was added to at least 3.125 μg oestrone, the mammary glands developed alveoli. The abnormalities produced by the highest doses of oestrone studied were exaggerated by the addition of testosterone. 4) The observations indicate a complicated interplay between the actions of testosterone and oestrone on the mammary gland of the rabbit. The interactions between testosterone and oestrone are presumably different from those observed between progesterone and oestrone.

EFFECT OF LOCALLY IMPLANTED OESTROGEN ON THE RESPONSE OF THE RAT'S LACTATING MAMMARY GLAND TO OXYTOCIN

1973 ◽  
Vol 73 (4) ◽  
pp. 700-712 ◽  
Author(s):  
J. D. Bruce ◽  
X. Cofre ◽  
V. D. Ramirez
Keyword(s):  
Mammary Gland ◽  
Mammary Glands ◽  
Myoepithelial Cells ◽  
Recording System ◽  
Saline Infusion ◽  
High Dose ◽  
Low Doses ◽  
Milk Ejection ◽  
Lactating Mammary Gland ◽  
Small Rise

ABSTRACT On the day following delivery (day 1 of lactation) one abdominal mammary gland was implanted with oestrogen and the contralateral gland received an empty needle. At 2, 5 or 10 days of lactation the rats were anaesthetized with pentobarbital and the nipples of both abdominal glands were cannulated and their pressures recorded by means of transducers coupled to an amplifier and recording system. The normal mammary glands of 5-day lactating rats responded to very low doses of oxytocin (Syntocinon®, Sandoz) (5× 10−8 mU) with a rhythmic elevation in pressure. However, saline infusion also evoked a small rise in intra-mammary pressure. Earlier (2 days) and later (10 days) in lactation the responses were smaller. Oestrogen decreases significantly the milk ejection response to oxytocin, and the effect was maximal at day 10 of lactation. Histological observations confirmed the diminished reaction of the gland to oxytocin, since the milk was retained in the alveoli of rats bearing a mammary-oestrogen implant. A paradoxical rise in pressure was detected in normal as well as in oestrogen-implanted glands when the lowest dose of oxytocin was injected in lactating rats which had previously received a high dose of oxytocin (50 mU or 500 mU). These results reinforce the hypothesis that oestrogen alters the milk ejection response to oxytocin and that the mechanism is probably related to changes in the contractility of the myoepithelial cells.

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