# Protective Effect of Oyaksoongi-San against Asthma Induced by Ovalbumin in a Mouse Model
## 4 Discussion  
In this study, we investigated the potential ability of OYSGS to inhibit asthma symptoms in an OVA-induced mouse model. In OVA-exposed mice, OYSGS was found to inhibit inflammatory cell recruitment and cytokine levels in BALF and lung tissues, reduce mucus production and oxidative stress, and attenuate p38 MAPK phosphorylation. Asthma is a chronic respiratory condition typified by enduring inflammation of the airways. It arises from a multifaceted interplay of diverse factors that act upon intricate pathogenic mechanisms. When administered in the respiratory system, ovalbumin acts as a specific allergen to provoke immune responses, including T-cell sensitization [46; 47]. Upon activation, T cells initiate a Th2 cell response that is characterized by phosphorylation of p38 MAPK, which, in turn, prompts the secretion of diverse pro-inflammatory cytokines [43; 44; 45; 48]. Key Th2 cell-secreted cytokines, such as IL-5 and IL-13, contribute to the induction of airway inflammation [27; 49]. Activated p38 MAPK may also recruit neutrophils and lymphocytes [50; 51]. At sites of inflammation, neutrophils rapidly infiltrate and function as significant modulators of both inflammation and immune responses [52]. Lymphocytes, including T cells and B cells, contribute to adaptive immunity [53]. Their recruitment regulates the production of cytokines and chemokines to intensity inflammation [54]. In the current study, OYSGS treatment of OVA-induced mice was found to notably diminish inflammatory cell infiltration into lung tissues, decrease inflammatory cell counts in BALF, and reduce pro-inflammatory cytokine levels in BALF. It can be inferred from these observations that OYSGS inhibits the inflammatory response associated with asthma. The asthma-related inflammatory response also leads to excessive mucus secretion. As mucus production increases, there are marked increases in the levels of glycoprotein in goblet cells and those of MUC5 AC within the airway [55; 56]. This heightened production of MUC5 AC in the airways is a hallmark of asthma [3]. Increased mucus production exacerbates airflow obstruction in several ways. Initially, the surplus mucus physically constricts the airway passages, complicating the flow of air in the lungs. The increased  
Figure 7: Effect of OYSGS on p38 MAPK activity in lung tissues. Phospho-p38 MAPK, p38 MAPK, and \(\beta\)-actin expression in lung tissues, as assessed by Western blotting. NC, negative control; OVA, ovalbumin-exposed mice; OVA+DEX, dexamethasone-administered and OVA-exposed mice; OVA+OYSGS100, OYSGS- (100 mg/kg) and OVA-exposed mice; OVA+OYSGS300, OYSGS- (300 mg/kg) and OVA-exposed mice; OVA+OYSGS500, OYSGS- (500 mg/kg) and OVA-exposed mice. Results are presented as means \(\pm\) SD (* \(p\) < 0.05, ** \(p\) < 0.01 compared with the OVA group). mucus also provides an ideal environment for the entrapment of airborne particles, such as allergens and pathogens, further contributing to worsened airway inflammation and bronchoconstrtion [57]. Moreover, the chronic presence of mucus provides a breeding ground for bacterial colonization, which can lead to recurrent infections and perpetuation of the inflammatory response [58]. Here, we show that OYSGS treatment of OVA-induced mice significantly reduced the lung levels of both glycoprotein and MUC5 AC expression, indicating that OYSGS inhibits asthma-related mucus production. In the context of asthma, excess oxidative stress is intimately linked to reactive oxygen species (ROS) in the lungs. Th2-generated p38 MAPK recruits infiltrated neutrophils, which release ROS to enhance tissue damage [8]. The increased oxidative stress caused by neutrophils leads to re-escalation of p38 MAPK phosphorylation, thereby enhancing the destructive response characteristic of asthma [59]. ROS can impair the lungs' natural antioxidant defenses, which, in turn, disrupts the balance of redox processes [60]. More specifically, ROS can harm cellular components, such as by causing lipid peroxidation, protein oxidation, and DNA histone modification [61].