The formula significantly inhibited the expression of TP53, HSP90AA1, and IL-17 mRNA, suggesting that it alleviates airway vascular remodeling and mucosal congestion in severe asthma by intervening in IL-17 A/F release mediated by Th17 cells, blocking CXCR2 signaling-driven neutrophil recruitment, and inhibiting IL-33-induced airway hyperresponsiveness. The gene discussed is CXCR2; the disease is airway hyperresponsiveness.