The pulmonary edema and inflammatory damage was largely related to the activation of the VIP/cAMP/PKA signal axis; therefore, the combined treatment would restore the expression of AQP-1 and AQP-5 proteins, inhibit the NF-κB and MAPK signaling pathways, inhibit the polarization of M1 macrophages, and promote the polarization of M2 macrophages. The gene discussed is NFKB1; the disease is edema.