Progesterone and estrogen influence postexercise leukocyte infiltration in overiectomized female rats

2008 ◽  
Vol 33 (6) ◽  
pp. 1207-1212 ◽  
Author(s):  
Sobia Iqbal ◽  
Amy Thomas ◽  
Kareem Bunyan ◽  
Peter M. Tiidus

Limited research has been conducted on the effects of progesterone alone, or in combination with estrogen, on leukocyte infiltration in skeletal muscle following exercise. To investigate the effects of these female sex hormones, ovariectomized female rats were divided into 4 exercise and 4 control groups: sham, estrogen, progesterone, and a combination of estrogen plus progesterone. Following 8 days of hormone replacement and 24 h postexercise, soleus (red) and superficial (white) vastus muscles were removed and immunostained for His48 (neutrophil)- and ED1 (macrophage)-positive cells. The postexercise increase in leukocyte infiltration was completely (p < 0.05) attenuated with estrogen supplementation alone in both muscle types, relative to sham. Progesterone treatment alone also resulted in a smaller (20%–30%) but significant (p < 0.05) attenuation of postexercise muscle leukocyte infiltration. The combination of estrogen and progesterone treatment did not significantly alter the attenuation seen with estrogen supplementation alone. Hence, progesterone can independently attenuate postexercise muscle leukocyte infiltration, albeit to a lesser degree than estrogen, and it will not negate or accentuate the effect of estrogen.

2017 ◽  
Vol 135 (1) ◽  
pp. 4-14 ◽  
Author(s):  
Raquel Prudente de Carvalho Baldaçara ◽  
Ivaldo Silva

ABSTRACT CONTEXT AND OBJECTIVE: The relationship between sex hormones and asthma has been evaluated in several studies. The aim of this review article was to investigate the association between asthma and female sex hormones, under different conditions (premenstrual asthma, use of oral contraceptives, menopause, hormone replacement therapy and pregnancy). DESIGN AND SETTING: Narrative review of the medical literature, Universidade Federal do Tocantins (UFT) and Universidade Federal de São Paulo (Unifesp). METHODS: We searched the CAPES journal portal, a Brazilian platform that provides access to articles in the MEDLINE, PubMed, SciELO, and LILACS databases. The following keywords were used based on Medical Subject Headings: asthma, sex hormones, women and use of oral contraceptives. RESULTS: The associations between sex hormones and asthma remain obscure. In adults, asthma is more common in women than in men. In addition, mortality due to asthma is significantly higher among females. The immune system is influenced by sex hormones: either because progesterone stimulates progesterone-induced blocking factor and Th2 cytokines or because contraceptives derived from progesterone and estrogen stimulate the transcription factor GATA-3. CONCLUSIONS: The associations between asthma and female sex hormones remain obscure. We speculate that estrogen fluctuations are responsible for asthma exacerbations that occur in women. Because of the anti-inflammatory action of estrogen, it decreases TNF-α production, interferon-γ expression and NK cell activity. We suggest that further studies that highlight the underlying physiopathological mechanisms contributing towards these interactions should be conducted.


Endocrinology ◽  
1939 ◽  
Vol 25 (4) ◽  
pp. 585-592 ◽  
Author(s):  
FRED W. CLAUSEN ◽  
CLAY B. FREUDENBERGER

2015 ◽  
Vol 93 (11) ◽  
pp. 993-998 ◽  
Author(s):  
Yuan Cheng ◽  
Qiaoying Li ◽  
Yidan Zhang ◽  
Quan Wen ◽  
Jianjun Zhao

Female sex hormones are considered to reduce the risk of ischemic stroke. As a part of the renin–angiotensin system, angiotensin-(1–7) [Ang-(1–7)] has recently been reported to play a role in protecting neuronal tissues from ischemic stroke. Thus, we examined the effects of female sex hormones on the levels of Ang-(1–7) and its downstream pathways in the brain. Female rats were ovariectomized and 17β-estradiol (17β-EST), progesterone (PGR), or a combination of 17β-EST plus PGR were administered. Our data demonstrated that lack of female sex hormones significantly decreased the levels of Ang-(1–7) in the cerebral cortex and hippocampal CA1 area. Also, we observed a linear relationship between cortex levels of Ang-(1–7) and plasma brain natriuretic peptide levels (as an indicator for risk of ischemic stroke). We further showed that lack of female sex hormones decreased the expression of Ang-(1–7), Mas-receptor (Mas-R), and neuronal nitric oxide synthase (nNOS). Overall, our findings show for the first time that Ang-(1–7) and Mas-R/nNOS in the cortex are influenced by circulating 17β-EST and (or) PGR, whereas Ang-(1–7) and its pathways in the hippocampal CA1 area are primarily altered by 17β-EST. This suggests that female sex hormones play a role in regulating the expression of Ang-(1–7) and its pathways during ischemic brain injuries.


2015 ◽  
Vol 10 (01) ◽  
pp. 65-71
Author(s):  
Chakorn Chansakul

2021 ◽  
pp. 105250
Author(s):  
Julia Strojny ◽  
Gregor Domes ◽  
Urs Fischbacher ◽  
Bernadette von Dawans

2014 ◽  
Vol 307 (2) ◽  
pp. R149-R157 ◽  
Author(s):  
Krystal N. Brinson ◽  
Olga Rafikova ◽  
Jennifer C. Sullivan

Initial studies found that female Dahl salt-sensitive (DS) rats exhibit greater blood pressure (BP) salt sensitivity than female spontaneously hypertensive rats (SHR). On the basis of the central role played by NO in sodium excretion and BP control, we further tested the hypothesis that blunted increases in BP in female SHR will be accompanied by greater increases in renal inner medullary nitric oxide synthase (NOS) activity and expression in response to a high-salt (HS) diet compared with DS rats. Gonad-intact and ovariectomized (OVX) female SHR and DS rats were placed on normal salt (NS; 0.4% salt) or HS (4% salt) diet for 2 wk. OVX did not alter BP in SHR, and HS diet produced a modest increase in BP. OVX significantly increased BP in DS rats on NS; HS further increased BP in all DS rats, although OVX had a greater increase in BP. Renal inner medullary NOS activity, total NOS3 protein, and NOS3 phosphorylated on serine residue 1177 were not altered by salt or OVX in either strain. NOS1 protein expression, however, significantly increased with HS only in SHR, and this corresponded to an increase in urinary nitrate/nitrite excretion. SHR also exhibit greater NOS1 and NOS3 protein expression than DS rats. These data indicate that female sex hormones offer protection against HS-mediated elevations in BP in DS rats but not SHR. We propose that the relative resistance to HS-mediated increases in BP in SHR is related to greater NOS expression and the ability to increase NOS1 protein expression compared with DS rats.


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