scholarly journals Phytoestrogens Enhance the Vascular Actions of the Endocannabinoid Anandamide in Mesenteric Beds of Female Rats

2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
Roxana N. Peroni ◽  
Tamara Abramoff ◽  
Isabel Neuman ◽  
Ernesto J. Podestá ◽  
Edda Adler-Graschinsky
Keyword(s):  
Estrogen Receptor ◽  
In Vitro Model ◽  
Oral Treatment ◽  
Concomitant Administration ◽  
Female Rats ◽  
Male Rats ◽  
Vascular Effects ◽  
Calcitonin Gene ◽  
Vitro Model

In rat isolated mesenteric beds that were contracted with NA as an in vitro model of the vascular adrenergic hyperactivity that usually precedes the onset of primary hypertension, the oral administration (3 daily doses) of either 10 mg/kg genistein or 20 mg/kg daidzein potentiated the anandamide-induced reduction of contractility to NA in female but not in male rats. Oral treatment with phytoestrogens also restored the vascular effects of anandamide as well as the mesenteric content of calcitonin gene-related peptide (CGRP) that were reduced after ovariectomy. The enhancement of anandamide effects caused by phytoestrogens was prevented by the concomitant administration of the estrogen receptor antagonist fulvestrant (2.5 mg/kg, s.c., 3 daily doses). It is concluded that, in the vasculature of female rats, phytoestrogens produced an estrogen-receptor-dependent enhancement of the anandamide-vascular actions that involves the modulation of CGRP levels and appears to be relevant whenever an adrenergic hyperactivity occurs.

477 Effect of Sexual Hormones On Cholinergic and Adrenergic Contractile Mechanisms of Colonic Smooth Muscle Strips in An In Vitro Model of NaïVe Female Rats

2008 ◽  
Vol 134 (4) ◽  
pp. A-64
Author(s):  
Bruno M. Balsiger ◽  
Thomas Hubacher ◽  
Christine Baumgartner ◽  
Luis A. Tovar ◽  
Christian Knusel ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
In Vitro Model ◽  
Female Rats ◽  
Sexual Hormones ◽  
Vitro Model

The effects of 17β-estradiol on blood brain barrier integrity in the absence of the estrogen receptor alpha; an in-vitro model

2017 ◽  
Vol 119 (6) ◽  
pp. 638-647 ◽  
Author(s):  
Serap Erdem Kuruca ◽  
Sabriye Karadenizli ◽  
Kadriye Akgun-Dar ◽  
Aysegul Kapucu ◽  
Zulal Kaptan ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Blood Brain Barrier ◽  
Estrogen Receptor Alpha ◽  
In Vitro Model ◽  
Barrier Integrity ◽  
Receptor Alpha ◽  
17Β Estradiol ◽  
Vitro Model ◽  
Blood Brain Barrier Integrity

scholarly journals An in vitro model for the effects of estrogen on neurons employing estrogen receptor-transfected PC12 cells

1994 ◽  
Vol 14 (6) ◽  
pp. 3945-3957 ◽  
Author(s):  
RH Lustig ◽  
P Hua ◽  
W Yu ◽  
FJ Ahmad ◽  
PW Baas
Keyword(s):  
Estrogen Receptor ◽  
Pc12 Cells ◽  
In Vitro Model ◽  
Vitro Model

scholarly journals Age Increase of Estrogen Receptor-α (ERα) in Cortical Astrocytes Impairs Neurotrophic Support in Male and Female Rats

Endocrinology ◽  
2013 ◽  
Vol 154 (6) ◽  
pp. 2101-2113 ◽  
Author(s):  
Jason M. Arimoto ◽  
Angela Wong ◽  
Irina Rozovsky ◽  
Sharon W. Lin ◽  
Todd E. Morgan ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Neurite Outgrowth ◽  
Female Rats ◽  
Male Rats ◽  
Neuronal Responses ◽  
Age Changes ◽  
Neurotrophic Activity ◽  
Cortical Astrocytes

Abstract Rodent models show decreased neuronal responses to estradiol (E2) during aging (E2-desensitization) in association with reduced neuronal estrogen receptor (ER)-α, but little is known about age changes of E2-dependent astrocytic neurotrophic support. Because elevated expression of astrocyte glial fibrillary acidic protein (GFAP) is associated with impaired neurotrophic activity and because the GFAP promoter responds to ERα, we investigated the role of astrocytic ERα and ERβ in impaired astrocyte neurotrophic activity during aging. In vivo and in vitro, ERα was increased greater than 50% with age in astrocytes from the cerebral cortex of male rats (24 vs 3 months), whereas ERβ did not change. In astrocytes from 3-month-old males, experimentally increasing the ERα to ERβ ratio induced the aging phenotype of elevated GFAP and impaired E2-dependent neurite outgrowth. In 24-month-old male astrocytes, lowering ERα reversed the age elevation of GFAP and partially restored E2-dependent neurite outgrowth. Mixed glia (astrocytes to microglia, 3:1) of both sexes also showed these age changes. In a model of perimenopause, mixed glia from 9- to 15-month rats showed E2 desensitization: 9-month regular cyclers retained young-like ERα to ERβ ratios and neurotrophic activity, whereas 9-month noncyclers had elevated ERα and GFAP but low E2-dependent neurotrophic activity. In vivo, ERα levels in cortical astrocytes were also elevated. The persisting effects of ovarian acyclicity in vitro are hypothesized to arise from steroidal perturbations during ovarian senescence. These findings suggest that increased astrocyte ERα expression during aging contributes to the E2 desensitization of the neuronal responses in both sexes.

In vitro hepatic deiodination of L-thyroxine to 3,5,3'-triiodothyronine in cold-acclimated rats

1980 ◽  
Vol 49 (3) ◽  
pp. 386-389 ◽  
Author(s):  
J. G. Scammell ◽  
K. T. Shiverick ◽  
M. J. Fregly
Keyword(s):  
Cold Acclimation ◽  
In Vitro Model ◽  
Male Rats ◽  
Incubation Periods ◽  
Adrenergic Activity ◽  
Serum T3 ◽  
Serum T4 ◽  
Liver Homogenates ◽  
Vitro Model

An in vitro model has been employed to evaluate the effect of cold acclimation on peripheral outer ring deiodination of thyroxine (T4) to triiodothyronine (T3) by 9,000 g supernatants of fresh liver homogenates. Hepatic T3 generation from T4 in male rats exposed to 4 +/- 1 degree C for 12 wk was 41 and 24% higher than control after 30- and 60-min incubation periods, respectively. This was associated with a 49% increase in serum T3 concentration in the cold-acclimated rats, whereas serum T4 concentration did not differ from the control. Thus, hepatic deiodination of T4 appears to serve as an important source for production of T3 during cold acclimation. It is suggested that the increased beta-adrenergic activity observed previously in cold-acclimated rats stimulates this change.

An in vitro model for investigation of vitamin A effects on wound healing

2021 ◽  
pp. 1-6
Author(s):  
Hoda Keshmiri Neghab ◽  
Mohammad Hasan Soheilifar ◽  
Gholamreza Esmaeeli Djavid
Keyword(s):  
Wound Healing ◽  
Endothelial Cell ◽  
Vitamin A ◽  
In Vitro Model ◽  
Cellular Proliferation ◽  
Endothelial Cell Migration ◽  
Normal Fibroblast ◽  
Anti Inflammatory ◽  
Vitro Model

Abstract. Wound healing consists of a series of highly orderly overlapping processes characterized by hemostasis, inflammation, proliferation, and remodeling. Prolongation or interruption in each phase can lead to delayed wound healing or a non-healing chronic wound. Vitamin A is a crucial nutrient that is most beneficial for the health of the skin. The present study was undertaken to determine the effect of vitamin A on regeneration, angiogenesis, and inflammation characteristics in an in vitro model system during wound healing. For this purpose, mouse skin normal fibroblast (L929), human umbilical vein endothelial cell (HUVEC), and monocyte/macrophage-like cell line (RAW 264.7) were considered to evaluate proliferation, angiogenesis, and anti-inflammatory responses, respectively. Vitamin A (0.1–5 μM) increased cellular proliferation of L929 and HUVEC (p < 0.05). Similarly, it stimulated angiogenesis by promoting endothelial cell migration up to approximately 4 fold and interestingly tube formation up to 8.5 fold (p < 0.01). Furthermore, vitamin A treatment was shown to decrease the level of nitric oxide production in a dose-dependent effect (p < 0.05), exhibiting the anti-inflammatory property of vitamin A in accelerating wound healing. These results may reveal the therapeutic potential of vitamin A in diabetic wound healing by stimulating regeneration, angiogenesis, and anti-inflammation responses.

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