Key result
Administration of RAS blockers largely rescued the increases in pro-fibrotic factors and RAS activation induced by ovariectomy in rats.
Why the study?
Oestrogen deficiency is linked with pulmonary fibrosis and may lead to over-activation of the renin-angiotensin system, which worsens lung fibrosis.
Do RAS blockers reduce lung fibrosis markers in ovariectomised rats with oestrogen deficiency?
Do RAS blockers reduce lung fibrosis markers in ovariectomised rats with oestrogen deficiency?
In a rat model, estrogen deficiency-induced lung fibrosis is mediated by the renin-angiotensin system and can be mitigated by RAS blockers.
Supports RAS blockade in estrogen-deficient rat lung fibrosis; hypothesis-generating, leaves open postmenopausal translation.
CONTEXT: Oestrogen deficiency is linked with pulmonary fibrosis. Additionally, it may lead to over-activation of the renin-angiotensin system (RAS), which worsens lung fibrosis. OBJECTIVE: The present study aims to investigate the role of RAS on lung fibrosis associated with oestrogen deficiency in ovariectomised rats. MATERIALS AND Moreover, lung tissues were examined by histopathology and immunohistochemistry. RESULTS: 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. CONCLUSION: Oestrogen deficiency activates RAS, which consequently increases the expression of pro-fibrotic factors and stimulates the fibrotic cascade causing lung fibrosis.
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Hussien et al. (2019) studied Lung fibrosis associated with oestrogen deficiency. RAS blockers vs. Ovariectomy without RAS blockers was evaluated on Lung fibrosis markers (hydroxyproline content, TGF-β1, plasma angiotensin II, ACE1, AT1R mRNA). Administration of RAS blockers largely rescued the increases in pro-fibrotic factors and RAS activation induced by ovariectomy in rats.
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