Chronic oestrogen deficiency induced by ovariectomy may cause lung fibrosis through activation of the renin-angiotensin system in rats

Oestrogen deficiency is linked with pulmonary fibrosis. Additionally, it may lead to over-activation of the renin-angiotensin system (RAS), which worsens lung fibrosis. The present study aims to investigate the role of RAS on lung fibrosis associated with oestrogen deficiency in ovariectomised rats....

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Bibliographic Details
Published in:Archives of physiology and biochemistry 2022-03, Vol.128 (2), p.290-299
Main Authors: Hussien, Noha I., El-kerdasy, Hanan I., Sorour, Safwa M., Shoman, Abeer A.
Format: Article
Language:English
Subjects:
aliskiren
Animals
Estrogens - adverse effects
Female
Humans
losartan
lung fibrosis
Oestrogen deficiency
Ovariectomy
Pulmonary Fibrosis - etiology
Pulmonary Fibrosis - metabolism
Rats
Receptor, Angiotensin, Type 1 - genetics
Receptor, Angiotensin, Type 1 - metabolism
Renin-Angiotensin System
TGF-β1
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Summary:Oestrogen deficiency is linked with pulmonary fibrosis. Additionally, it may lead to over-activation of the renin-angiotensin system (RAS), which worsens lung fibrosis. The present study aims to investigate the role of RAS on lung fibrosis associated with oestrogen deficiency in ovariectomised rats. Serum 17 β -oestradiol (E2), arterial blood gases, plasma angiotensin II levels, lung tissue hydroxyproline content, and transforming growth factor beta 1 (TGF-β1) concentration, the mRNA expression of angiotensin type 1 receptor (AT1R), and angiotensin-converting enzyme (ACE1) were evaluated. Moreover, lung tissues were examined by histopathology and immunohistochemistry. Hydroxyproline content, TGF-β1 concentration, plasma angiotensin II, the relative mRNA expression of ACE1, and AT1R is found to increase in ovariectomised rats. The mentioned changes can be largely rescued by administration of RAS blockers. Oestrogen deficiency activates RAS, which consequently increases the expression of pro-fibrotic factors and stimulates the fibrotic cascade causing lung fibrosis.
ISSN:1381-3455
1744-4160
DOI:10.1080/13813455.2019.1676262