Especially, quercetin, luteolin, kaempferol, tanshinone IIA, and baicalein were the main effectors in YQJPR, which primarily downregulated the expressions of five key targets (MAPK3, AKT1, MYC, STAT3, and CASP3), and subsequently inhibited the activation of virus infection, cancer, MAPK, HIF-1, TNF, and IL-17 pathways, thereby alleviating CS/LPS-induced lung inflammation. This evidence concerns the gene HIF1A and viral infectious disease.