Document Type : Original Article
Author
Department of Medical Pharmacology, Faculty of Medicine, Cairo University, Egypt.
Abstract
Background: Bronchial asthma is a progressive and disability disease. Most treatment lines of bronchial asthma still act as bronchodilators and anti-inflammatory drugs rather than treating underlying disease pathogenesis so new drug classes are needed to be tested as primary goals. Angiotensin II is potentially implicated in its pathogenesis, being a potent pro-inflammatory mediator with remodeling effects. Aim: To study potential beneficial effect of telmisartan, an angiotensin II receptor blocker, on experimentally induced bronchial asthma in rats. Patients and Methods: 30 male Sprague Dawley rats were divided into 5 groups; a normal control group, an asthma control group, a dexamethasone treated group, telmisartan treated groups and salbutamol treated group. Bronchial asthma was induced by intraperitoneal sensitization followed by intranasal challenge with ovalbumin (OVA). PULMONARY function tests were assessed 1 h after the last challenge. One day after the last challenge, absolute eosinophil counts (AEC) in blood and bronchoalveolar lavage fluids (BALF), Serum and BALF immunoglobulin E, total nitrate/nitrite (NOx), Oxidative and inflammatory biomarkers, lung tissue superoxide dismutase (SOD), glutathione reduced (GSH), tumor necrosis factor-alpha (TNF-a) and interleukin-5 (IL-5), were assessed, in addition to histopathological study. Results: Telmisartan significantly improved TV, PEF, AEC, IgE, NOx, GSH, SOD, TNF-a and IL-5 values compared to asthma control values. Histopathological study runs in parallel to biochemical results showing normal lung architecture in telmisartan treatment. Relation between patient’s results and types of graft used showed no statistically significant differences between them. Conclusion: These results shows that telmisartan ameliorate bronchial asthma as regarding biochemicals and histological results due to its bronchodilator, antioxidant, and anti-inflammatory effects.
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