Abstract
Ravan Napas (RN) is a traditional formula used to treat pulmonary symptoms and diseases such as coughing, breathing difficulty, and asthma in traditional Uighur medicine. The purpose of this study was to investigate the anti-inflammatory, and immuno-modulatory activity of RN in a well-characterized animal model of allergic asthma. Rats were sensitized with intraperitoneal (ip) ovalbumin (OVA) and alum, and then challenged with OVA aerosols. The asthma model rats were treated with RN; saline- and dexamethasone- (DXM-) treated rats served as normal and model controls. The bronchoalveolar lavage fluid (BALF) cellular differential and the concentrations of sICAM-1, IL-4, IL-5, TNF-α, INF-γ, and IgE in serum were measured. Lung sections underwent histological analysis. The immunohistochemistry S-P method was used to measure the expression of ICAM-1 and HO-1 in the lung. RN significantly reduced the number of inflammatory cells in BALF and lung tissues, decreased sICAM-1, IL-4, IL-5, TNF-α, and IgE in serum, and increased serum INF-γ. There was a marked suppression of ICAM-1 and HO-1 expression in the lung. Our results suggest that RN may have an anti-inflammatory and immuneregulatory effect on allergic bronchial asthma by modulating the balance between Th1/Th2 cytokines.
Highlights
Asthma is a major public health problem worldwide
The lung tissue obtained from ovalbumin-induced asthmatic rats was characterized by dense peribronchial inflammation due to leukocyte infiltration and mucus hyperproduction by goblet cells within the bronchi when compared with normal tissue
A rat model of allergic asthma was developed, the lung tissues examined, and BAL analysed to assess the effect of Ravan Napas (RN) on airway inflammation in experimental asthma
Summary
Asthma is a major public health problem worldwide. Asthma morbidity and mortality have increased in the recent decades [1]. Bronchial asthma is a chronic inflammatory disorder of the airways characterized by airflow obstruction, airway inflammation, persistent airway hyperresponsiveness (AHR), and airway remodeling [2]. Increasing evidence suggests that many cells and cellular elements play prominent roles in the pathogenesis of allergic asthma [3, 4]. This pathogenesis is mediated by nonspecific infiltration by various inflammatory cells such as eosinophils, T-lymphocytes, macrophages, neutrophils, and epithelial cells [5, 6]. Symptoms are mediated by a wide range of compounds such as histamine, cytokines, and cyclo-oxygenase and lipoxygenase products [7]
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