## 4 Discussion  
Allergic rhinitis, a hypersensitivity immune disorder, is a common inflammatory disease that affects all age groups [17]. Approximately 10% of the world population suffers from AR, and its incidence has been observed to rise rapidly every year [2,18]. Patients of AR present with symptoms including itching, runny nose, and sneezing, which can significantly affect functionality [19]. Many studies have demonstrated that Th-2 mediated cytokines play a critical role in allergic inflammatory rhinitis and the importance of the relationship between Th-2 cells and allergic rhinitis is well established [20]. Activated Th-2 cell secrete signal molecules including TNF, IL-4, and IL-13 that activate B cells and mast cells. Post this induction, activated B cells produce IgE that stimulates mast cells and basophils, leading to an allergic reaction. Furthermore, Th-2 cells activate eosinophils via IL-3 or IL-5, resulting in cell migration into the vascular endothelium. Therefore, inhibition of an upstream pathway such as the Th-2 signaling pathway in allergic response may result in a better clinical outcome as compared to inhibition of downstream steps in the inter-related signal transduction pathways [21]. Previous studies show that TSLP, IL-25, and IL-33, which are produced in epithelial cells, are critical Th-2 differentiators [22]. Allergens or chemicals can promote protein arginine methyltransferase 1(PRMT1) expression via mitogen-activated protein kinase (MAPK) phosphorylation in epithelial cells, which in turn can stimulate Th-2 cells, Mast cells, and type 2 innate lymphoid (ILC2) cells via secreted TSLP, IL-25, and IL-33. During this process, elevated IL-4, IL-5, and IL-13 levels lead to eosinophil and mast cell degranulation, IgE synthesis from B cells, and the subsequent development of a characteristic type 2 immune environment [23,24]. In this study, we used an allergic rhinitis mouse model that, on induction with OVA-inhalation, showed pathological changes associated with AR including nasal itching and sneezing, as reported previously [25]. We observed sensitization and challenge with OVA-induced allergic rhinitis and a concomitant significant increase in immunocytes populations, including eosinophils and basophils in serum. Furthermore, the oral administration of CIAR at three incremental doses resulted in the alleviation of immunocyte levels in a dose-dependent manner. ECP is a cytotoxic protein granule produced by eosinophils \begin{table}
\begin{tabular}{c c c} \hline \hline  & **CI** & **AR** \\ \hline Quercetin & 4.2 \(\pm\) 0.67 & 7.3 \(\pm\) 0.71 \\ Kaemferol & 2.5 \(\pm\) 0.42 & 2.1 \(\pm\) 0.78 \\ Isorhametic & N.D. & N.D. \\ \hline \hline \end{tabular} N.D.—non-detected.  
\end{table} 
Table 4: Contents of flavonoids in CI and AR. \begin{table}
\begin{tabular}{c c c} \hline \hline  & **CI** & **AR** \\ \hline P-Ser & 133.5 \(\pm\) 6.7 & 340.5 \(\pm\) 13.6 \\ Asp & 81.56 \(\pm\) 10.5 & 894.5 \(\pm\) 3.4 \\ Thr & N.D. & 405.5 \(\pm\) 3.4 \\ Glu & N.D. & 1079.1 \(\pm\) 13.6 \\ Gly & N.D. & 131.9 \(\pm\) 3.4 \\ Ala & N.D. & 1899.3 \(\pm\) 6.8 \\ Val & 227.4 \(\pm\) 7 & 1052.8 \(\pm\) 3.4 \\ Cys & N.D. & 64.8 \(\pm\) 3.4 \\ Ile & N.D. & 136.7 \(\pm\) 3.4 \\ Leu & N.D. & 417.3 \(\pm\) 6.8 \\ Phe & N.D. & 4125.5 \(\pm\) 6.78 \\ g-ABA & 180.4 \(\pm\) 3 & 1148.7 \(\pm\) 3.4 \\ \hline \hline \end{tabular} P-ser—phosphoserine; Asp—asparadic acid; Thr—thereonine; Glu—glutamic acid; Gly—glycine; Ala—alanine; Val— valine; Cys—cystine; Ile—soleucine; Leu—leucine; Phe—phenylalanine; g-ABA—g-amino-n-butyric acid; N.D.—non-detected.  
\end{table} 
Table 3: Contents of amino acids in CI and AR. and may play a role in the pathophysiology of allergic rhinitis, such as epithelial cell damage and non-specific hyperreactivity [26]. We were able to demonstrate an elevation in serum ECP post OVA inhalation, which was reversed by the administration of CIAR in a dose-dependent manner.