## 1 Introduction  
Allergic asthma is a chronic inflammatory respiratory disease characterized by hypersensitivity of the respiratory tract to various allergens and irritants [1]. It is marked by the infiltration of eosinophils into the airways, leading to bronchiolar constriction,increased airway hyperresponsiveness, excessive mucus production, and elevated immunoglobulin E (IgE) levels, along with significant goblet cell hyperplasia [2; 3]. The global prevalence of allergic asthma has been rising, particularly in developing countries with higher levels of air pollution [4]. The key signaling pathways implicated in allergic asthma include nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB), phosphoinositide 3-kinase/protein kinase B (PI3K/Akt), and p38 mitogen-activated protein kinases (MAPK) [5; 6; 7]. Additionally, Type 2 helper T (Th2) cells and related cytokines like interleukin (IL)-4, IL-5, and IL-13 play a crucial role in asthma pathogenesis [8; 9; 10]. Among these, IL-4 is responsible for driving allergic inflammation and airway remodeling by promoting the differentiation of IgE-producing B lymphocytes [11; 12]. IL-5, on the other hand, is specific to eosinophil leukocytes and plays a critical role in their proliferation, differentiation, migration, activity, recruitment, and survival [13]. The accumulation of eosinophil leukocytes in tissue contributes to various allergic reactions, including asthma [14]. As a result, the regulation of IL-4 or IL-5 has emerged as a significant target in the development of therapeutic agents for allergic asthma [15; 16]. Currently, the most commonly employed treatments for asthma involve the inhalation of \(\beta\)2 receptor agonists or the inhalation and oral administration of glucocorticoids. However, their prolonged usage is constrained by the fact that they fail to address the root cause of asthma and are associated with diverse side effects [17]. Consequently, there exists a compelling need to formulate novel asthma treatment options that exhibit a comparatively reduced incidence of side effects while delivering heightened efficacy [18]. Within the realm of corticosteroids, dexamethasone (DEXA) stands out as one of the extensively utilized benchmark drugs in the progression of new asthma therapies [19; 20; 21; 22]. Therefore, this study employs DEXA (0.75 mg/kg) as a control substance. This selection has been reported by a wide array of respiratory disease models available for evaluating drug efficacy, including allergic asthma [20; 21; 22; 23]. The ovalbumin (OVA) sensitization and re-exposure (boosting) induced C57 BL/6 mouse asthma model ranks among the extensively employed experimental animal models for assessing the effectiveness of asthma treatment candidates. This model is preferred due to its capability to induce distinct allergic asthmatic symptoms in animals within a mere three days subsequent to the topical re-exposure to OVA [20; 21; 24]. Through the utilization of this animal model, drug efficacy has primarily been gauged by monitoring alterations in the lung weight, the levels of inflammatory cytokines in lung tissue and the bloodstream, and the presence of cellular components like eosinophils and neutrophils within the bronchoalveolar lavage fluid (BALF). Additionally, a histopathological examination of the airways, encompassing the lungs, constitutes an essential aspect of this evaluation process [20; 21; 24]. Bioactive compounds derived from natural sources are renowned for their ability to elicit relatively low side effects while demonstrating exceptional anti-inflammatory and antioxidant properties [25; 26]. Consequently, the development of respiratory protective drugs using natural substances within diverse asthma experimental animal models, including OVA-induced C57 BL/6 mice, is currently advancing [20; 21; 22]. Among the spectrum of natural products, peers (_Pyrus_ spp.) stand out as one of the most frequently consumed fruits worldwide [27].