Search In this Thesis
   Search In this Thesis  
العنوان
Potential effects of rosuvastatin on bleomycin-induced pulmonary fibrosis /
المؤلف
Harb, Marwa Fathy Ibrahim.
هيئة الاعداد
باحث / مروة فتحي إبراهيم حرب
مشرف / عبدالرحمن عبدالفتاح يس
مشرف / عبدالمتعال مصطفى فودة
مشرف / نبيل محمود عبدالخالق الأديب
الموضوع
Lung Diseases. physiopathology. Lung - anatomy & histology. Cystic fibrosis. Pulmonary fibrosis. Pulmonary fibrosis - diagnosis. Pulmonary fibrosis - etiology.
تاريخ النشر
2020.
عدد الصفحات
online resource (127 pages) :
اللغة
الإنجليزية
الدرجة
ماجستير
التخصص
الطب
تاريخ الإجازة
1/1/2020
مكان الإجازة
جامعة المنصورة - كلية الطب - قسم الفارماكولوجيا الإكلينيكية
الفهرس
Only 14 pages are availabe for public view

from 127

from 127

Abstract

Background: Idiopathic pulmonary fibrosis (IPF) is a chronic and progressive interstitial lung disease, characterized by abnormal extracellular matrix deposition. The exact etiology is poorly understood, involving a variety of cellular processes, signaling pathways, and genetics. IPF is manifested by progressive dyspnea and cough, which lead to reduced quality of life and ultimately respiratory failure and death. Despite considerable progress in IPF medical treatment, the only effective therapy is lung transplantation, which is however burdened by significant risks of complications and death. Pirfenidone was approved as an anti-fibrotic agent in IPF. Although it has improved IPF clinical management considerably, it only slows lung function decline and can’t halt or regress fibrosis progression. Statins are usually prescribed as a lipid- lowering medication, and there is accumulating evidence that statins have multiple secondary effects, both related and unrelated to their lipid-lowering effect. They are commonly prescribed and relatively-safe drugs, making them a charming treatment option for fibrosis. The aim of the work: To test the potential ‘therapeutic’ effect of rosuvastatin on bleomycin-induced pulmonary fibrosis in mice; by assessing mouse body weight, lung weight, lung index and lung histopathological scoring. Also, it aims to compare the resultant effect of rosuvastatin with the well-established anti-fibrotic effect of pirfenidone, with focusing on transforming growth factor-β1 (TGF-β1) as a master marker of fibrosis. Materials and Methods: For induction of pulmonary fibrosis, C57BL/6 mice were intra-tracheally injected with bleomycin (2U/Kg, 50 μl), considering that day as day zero (day 0). Then, at the tenth day (day 10), mice of pirfenidone group or rosuvastatin group were started to orally receive pirfenidone (300mg/kg/d) or rosuvastatin (10mg/kg/d) drugs, respectively for each group. Finally, at day twenty-one (day 21), all mice were sacrificed. Final body weight, lung weight, lung index and lung TGF-β1were measured. Also, histopathological examination of lung sections was done; using HE staining and Masson’s trichrome staining; the latter stain was used for scoring fibrosis.