scholarly journals Topical Estrogen Therapy for Hyperopia Correction in Vivo

2020 ◽  
Vol 61 (6) ◽  
pp. 55
Author(s):  
Ari Leshno ◽  
Katalin Prokai-Tatrai ◽  
Ygal Rotenstreich ◽  
Asaf Magid ◽  
Ettel Bubis ◽  
...  
Keyword(s):  
Estrogen Therapy ◽  
Topical Estrogen

Topical Estrogen Therapy for Androgenetic Alopecia in Menopausal Females

Dermatology ◽  
2004 ◽  
Vol 208 (2) ◽  
pp. 178-179 ◽  
Author(s):  
S. Georgala ◽  
A.C. Katoulis ◽  
C. Georgala ◽  
V. Moussatou ◽  
E. Bozi ◽  
...  
Keyword(s):  
Estrogen Therapy ◽  
Androgenetic Alopecia ◽  
Topical Estrogen

Abstract 285: Cardiac Inflammation and Fibrosis Induced by Heart Failure Are Reversed by Short-Duration Estrogen Therapy

2012 ◽  
Vol 111 (suppl_1) ◽  
Author(s):  
Andrea Iorga ◽  
Rangarajan Nadadur ◽  
Salil Sharma ◽  
Jingyuan Li ◽  
Mansoureh Eghbali
Keyword(s):  
Heart Failure ◽  
Estrogen Therapy ◽  
Pressure Overload ◽  
Decompensated Heart Failure ◽  
Left Ventricular ◽  
Neonatal Rat ◽  
In Vivo Model ◽  
Anti Inflammatory

Heart failure is generally characterized by increased fibrosis and inflammation, which leads to functional and contractile defects. We have previously shown that short-term estrogen (E2) treatment can rescue pressure overload-induced decompensated heart failure (HF) in mice. Here, we investigate the anti-inflammatory and anti-fibrotic effects of E2 on reversing the adverse remodeling of the left ventricle which occurs during the progression to heart failure. Trans-aortic constriction procedure was used to induce HF. Once the ejection fraction reached ∼30%, one group of mice was sacrificed and the other group was treated with E2 (30 αg/kg/day) for 10 days. In vitro, co-cultured neonatal rat ventricular myocytes and fibroblasts were treated with Angiotensin II (AngII) to simulate cardiac stress, both in the presence or absence of E2. In vivo RT-PCR showed that the transcript levels of the pro-fibrotic markers Collagen I, TGFβ, Fibrosin 1 (FBRS) and Lysil Oxidase (LOX) were significantly upregulated in HF (from 1.00±0.16 to 1.83±0.11 for Collagen 1, 1±0.86 to 4.33±0.59 for TGFβ, 1±0.52 to 3.61±0.22 for FBRS and 1.00±0.33 to 2.88±0.32 for LOX) and were reduced with E2 treatment to levels similar to CTRL. E2 also restored in vitro AngII-induced upregulation of LOX, TGFβ and Collagen 1 (LOX:1±0.23 in CTRL, 6.87±0.26 in AngII and 2.80±1.5 in AngII+E2; TGFβ: 1±0.08 in CTRL, 3.30±0.25 in AngII and 1.59±0.21 in AngII+E2; Collagen 1: 1±0.05 in CTRL.2±0.01 in AngII and 0.65±0.02 (p<0.05, values normalized to CTRL)). Furthermore, the pro-inflammatory interleukins IL-1β and IL-6 were upregulated from 1±0.19 to 1.90±0.09 and 1±0.30 to 5.29±0.77 in the in vivo model of HF, respectively, and reversed to CTRL levels with E2 therapy. In vitro, IL-1β was also significantly increased ∼ 4 fold from 1±0.63 in CTRL to 3.86±0.14 with AngII treatment and restored to 1.29±0.77 with Ang+E2 treatment. Lastly, the anti-inflammatory interleukin IL-10 was downregulated from 1.00±0.17 to 0.49±0.03 in HF and reversed to 0.67±0.09 in vivo with E2 therapy (all values normalized to CTRL). This data strongly suggests that one of the mechanisms for the beneficial action of estrogen on left ventricular heart failure is through reversal of inflammation and fibrosis.

scholarly journals PIH2 Topical Estrogen Therapy in Postmenopausal Women - Indian Experience

2012 ◽  
Vol 15 (7) ◽  
pp. A638
Author(s):  
S. Donde ◽  
G. Uchit ◽  
N. Valanju
Keyword(s):  
Postmenopausal Women ◽  
Estrogen Therapy ◽  
Indian Experience ◽  
Topical Estrogen

A randomized comparative study of the effects of oral and topical estrogen therapy on the vaginal vascularization and sexual function in hysterectomized postmenopausal women

2006 ◽  
Vol 13 (5) ◽  
pp. 737-743 ◽  
Author(s):  
Cheng-Yu Long ◽  
Cheng-Min Liu ◽  
Shih-Cheng Hsu ◽  
Chin-Hu Wu ◽  
Chiu-Lin Wang ◽  
...  
Keyword(s):  
Comparative Study ◽  
Sexual Function ◽  
Postmenopausal Women ◽  
Estrogen Therapy ◽  
Topical Estrogen

scholarly journals Formulation and Evaluation of Herbal Hair Gel Containing Fenugreek Seed Extract for Nourishment and Hair Growth

2019 ◽  
pp. 92-103
Author(s):  
Suryawanshi Nishant C ◽  
Vijayendra Swamy S. M. ◽  
Nagoba Shivappa N. ◽  
Wanje Vaijanti V.
Keyword(s):  
Hair Loss ◽  
Hair Growth ◽  
Estrogen Therapy ◽  
Hair Follicles ◽  
Hormone Deficiency ◽  
Gelling Agent ◽  
Nutritional Deficiencies ◽  
Topical Formulation ◽  
Fenugreek Seed

The present study now a days many people face the major problem related to hair i.e. hair loss. There are many causes of hair loss physiological conditions, emotional or physical stress, nutritional deficiencies, hormonal disorders one of the due to hormone deficiency of estrogen. External administration of the estrogen could changes the hormonal cycle and increase cancer risk some natural alternative estrogen therapy can be found in the various plants containing natural products those having weak estrogen activity like Phyto-estrogen. Herbal drug has less side effects and more effective as comparative to synthetic drug. Phytoestrogen are competing with the estrogen by the binding to the estrogen receptor and produce estrogen effect, Phytoestrogen in the fenugreek seed. Family – Fabaceae Ethanolic extract of (Trigonella foenum-graecum) fenugreek seed prepared for the topical formulation of herbal hair gel formulation by using Carbopol 934 gelling agent, glycerin, pvp, methyl paraben, PEG, Triethanolamine Fenugreek was evaluated for its potency on hair growth activity by in vivo method. In vivo, study 2.5mg of fenugreek extract is used. That is applied on the shaved skin of mice to determine the length of hair and the different cyclic phase of hair follicles like anagen and s phases were will be grow after some time periods. From the study topical use of gel formulation were apply for 30 days .There are use of fenugreek extract containing gel formulation over the shaved skin of mice that shows the significant result by increase the hair growth. The prepared gel was characterized for their physicochemical constants, preliminary phyto-chemical analysis, quantitative analysis, Spread-ability, pH, viscosity, and stability study.

Phyto-anti-estrogens are potential selective modifiers of biological reactions in breast cancer

2016 ◽  
Vol 21 (4) ◽  
pp. 212-219 ◽  
Author(s):  
Juliya A. Borisova ◽  
G. B Smirnova ◽  
I. Zh Shubina ◽  
Z. S Shprakh ◽  
E. M Treshchalina
Keyword(s):  
Breast Cancer ◽  
Proliferative Activity ◽  
Estrogen Therapy ◽  
Therapeutic Agents ◽  
Mechanisms Of Action ◽  
Present Knowledge ◽  
Estrogen Action ◽  
In Vivo Models ◽  
Positive Breast Cancer

The review analyzes up-to-date information about specific characteristics of anti-estrogen therapeutic agents with different mechanisms of action with regard to present knowledge of endocrine therapy for estrogen-positive breast cancer (ER+ BC). The paper presents some agents for anti-estrogen therapy of breast cancer - aromatase inhibitors and selective modifiers of biological reactions (SMBR) and their mechanisms of anti-proliferative action. The authors describe significant therapeutic and side effects as well as different options for anti-estrogen combinations. Special emphasis is made on national herbal estrogens/anti-estrogens that have no toxicity associated with the well-known SMBRs. The review presents the structure and characteristics of a perspective phyto-anti-estrogen sekoizolaricirezinol (SEKO), which demonstrated significant anti-proliferative activity with no pro-estrogen action in the in vivo models of ER+ BC.

Topical estrogen therapy in the management of postmenopausal vaginal atrophy: an up-to-date overview

Climacteric ◽  
2009 ◽  
Vol 12 (2) ◽  
pp. 91-105 ◽  
Author(s):  
O. Al-Baghdadi ◽  
A. A. A. Ewies
Keyword(s):  
Estrogen Therapy ◽  
Vaginal Atrophy ◽  
Topical Estrogen

New developments in topical estrogen therapy

1997 ◽  
Vol 67 (1) ◽  
pp. 1-12 ◽  
Author(s):  
Raphael Jewelewicz
Keyword(s):  
Estrogen Therapy ◽  
New Developments ◽  
Topical Estrogen

Abstract 185: Androgen Deficiency-induced Hyperplasia Development is Attenuated by Physiological Testosterone Replacement Independent of Metabolite Dihydrotestosterone

2016 ◽  
Vol 36 (suppl_1) ◽  
Author(s):  
Junior Univers ◽  
Brian M Freeman ◽  
Deidra J Mountain ◽  
Stacy S Kirkpatrick ◽  
Joshua D Arnold ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Hormone Replacement ◽  
Estrogen Therapy ◽  
In Vivo Model ◽  
Androgen Deficiency ◽  
Post Injury ◽  
Estrogen Receptor Signaling ◽  
Increased Risk

Objectives: Androgen deficiency (AD) is associated with increased risk of cardio- and peripheral vascular disease, yet the underlying biochemical mechanisms remain unclear. Systemically testosterone (TST) is enzymatically reduced to its more potent metabolite dihydrotestosterone (DHT) or is aromatized to estradiol, which differentially stimulate androgen and estrogen receptor-mediated pathways, respectively. We have previously demonstrated an inverse relationship between TST levels and the cellular processes of intimal hyperplasia (IH) in vitro. Here we investigated TST and DHT replacement in the attenuation of IH in an in vivo model of AD. Methods: Sub- to high physiologic levels of TST or DHT was administered via pellet implants in aged orchiectomized rats (0.5-5mg). Young intact (YI), aged intact (AI), and orchiectomized placebo (Plac) rats served as controls. After 14d hormone replacement rats underwent balloon angioplasty of the left common carotid. 14d post-injury animals were euthanized, systemic hormone levels were determined by ELISA and comparative weight analysis of androgen sensitive organs (Table 1), and carotid intima:media (I:M) was quantified. Results: I:M was decreased in AI animals and with higher physiological TST replacement compared to YI controls (Fig 1). I:M was higher in Plac, sub- and low-physiological TST animals and at all DHT levels. Conclusions: Aging and the normal reduction of TST was protective against IH when compared to young animals. However, pathological AD and sub-physiological hormone replacement increased IH. While physiological TST replacement attenuated this effect, equivalent DHT replacement was not protective, but instead exacerbated the hyperplastic response. Future studies will investigate if the protective effect of physiological TST replacement could be via its conversion to estradiol and downstream estrogen receptor signaling and if estrogen therapy attenuates IH in AD males.

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