## 4 Discussion
In contrast, compared to the OVA control group, the IAP-extract-administered groups showed significant and dose-dependent increases in the ASA, the average alveolar septal thickness, infiltrating inflammatory cells within the alveoli and peribronchiolar regions, eosinophilic leukocytes, and mast cell numbers. These findings provide compelling direct evidence suggesting that the oral administration of IAP extract has the potential to suppress OVA-induced allergic asthma in a dose-dependent manner through its anti-inflammatory effects. NF-\(\kappa\)B, a crucial player in inflammation linked to reactive oxygen species (ROS), exerts its effects by binding to promoters encoding tumor necrosis factor (TNF)-\(\alpha\), ILs (IL-1 and IL-6), and certain adhesion molecules [62; 63]. Moreover, NF-\(\kappa\)B regulates the expression of various cytokines that are directly involved in the inflammatory response [64; 65]. Its overexpression is well documented in allergic asthma, and the upregulation of p38 MAPK, PI3K, and Akt is also observed alongside an increase in NF-\(\kappa\)B expression [5; 66; 7; 5; 67]. Furthermore, PTEN serves as a pivotal suppressor of tumorigenesis within the PI3K/Akt signaling pathway. Abnormalities in the PTEN gene contribute to the pathogenesis of various malignancies [68; 69; 70]. PTEN gene expression is modulated by the MAPK signaling pathway [71], where inhibiting the MAPK signaling pathway substantially curtains malignant tumor development by maintaining PTEN expression [70; 72]. Currently, the enhanced PTEN expression or suppression of PI3K activity has emerged as a potential strategy to alleviate allergic asthma through the regulation of various signal transduction pathways [66; 73; 74]. In this study, OVA sensitization and local re-exposure through nasal administration led to a significant increase in oxidative stress and inflammation-related NF-kB, p38 MAPK, PI3K, and Akt mRNA expressions, coupled with a decrease in PTEN mRNA expression within lung tissue. Conversely, a dose-dependent attenuation of oxidative stress-induced inflammatory lung damage was evident through the modulation of OVA-induced PI3K/AKT/PTEN, p38 MAPK, and NF-kB mRNA expressions in all three doses of IAP-administered groups. The findings of this study collectively provide compelling evidence supporting the potential of the oral administration of IAP extract in the dose-dependent mitigation of OVA-induced allergic asthma, oxidative stress, and inflammatory lung damage. This effect is likely medicated through the anti-inflammatory and antioxidant activities, achieved by regulating key signaling pathways including p38 MAPK, NF-kB, and PI3K/Akt/PTEN. Nevertheless, it is important to acknowledge the several limitations of this study. Further research could delve deeper into elucidating the specific mechanisms by which IAP extract influences the PI3K-Akt pathway, possibly involving phosphorylation events, in the context of the OVA-induced in vivo asthma model. Additionally, conducting electron microscopic studies on lung tissues might offer valuable insights into the ultrastructural changes underlying the observed effects. While the present study contributes valuable insights into asthma research, it is essential to recognize that further rigorous clinical studies are necessary to corroborate these findings before considering the incorporation of Asian pear extract into health-functional foods or pharmaceutical products.