أعضاء هيئة التدريس - جامعة بنها
Chronic oestrogen deficiency induced by ovariectomy may cause lung fibrosis through activation of the renin-angiotensin system in rats
• 2019
معلومات البحث
المؤلفون
Noha I. Hussien, Hanan I. El-kerdasy, Safwa M. Sorour & Abeer A. Shoman
الكلمات المفتاحية
Oestrogen deficiency; lung
fibrosis; renin-angiotensin
system; TGF-b1;
losartan; aliskiren
المجلة العلمية
Not Available
الناشر
Not Available
المجلد
Not Available
العدد
Not Available
الصفحات
Not Available
publication.type
International
رابط البحث
Not Available
المواد المرفقة
Not Available
الملخص
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 methods: Serum 17b-oestradiol (E2), arterial blood gases, plasma angiotensin II levels,
lung tissue hydroxyproline content, and transforming growth factor beta 1 (TGF-b1) 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.
Results: Hydroxyproline content, TGF-b1 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.
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 methods: Serum 17b-oestradiol (E2), arterial blood gases, plasma angiotensin II levels,
lung tissue hydroxyproline content, and transforming growth factor beta 1 (TGF-b1) 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.
Results: Hydroxyproline content, TGF-b1 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.