Abstract: OBJECTIVE To explore the mechanism of epigallocatechin gallate(EGCG) inhibit influenza A virus H1N1 replication through inducing production of IFN-β by the p38 signaling factor. METHODS EGCG was applied to human tubular epithelial cells(BEAS-2B), the expression of IFN-β mRNA and protein in BEAS-2B was detected by qRT-PCR and ELISA, and the expression of p38 and p-p38 protein was detected by Western blotting. Used p38 inhibitors to inhibit the signal transduction of p38 signal factors, and detected the effect of EGCG on BEAS-2B cells to induce the expression of IFN-β protein and mRNA. IFN-β antibody was used to neutralize the production of IFN-β in cells, and the expression of NP protein and mRNA after EGCG treated H1N1 was detected by qRT-PCR and Western blotting. RESULTS Compared with EGCG(0 μg·mL^-1), as the dose of EGCG increased, IFN-β protein and mRNA increased significantly. Compared with 0 h of treatment, EGCG(20 μg·mL^-1) induced significant IFN-β protein expression when cells were treated for 12 h(P<0.01). EGCG could promote the phosphorylation of p38 in BEAS-2B; after the use of p38 inhibitors to inhibit the p38 signaling pathway, EGCG induced a decrease in IFN-β mRNA and protein expression(P<0.01). Compared with EGCG alone in the treatment of H1N1 cells, the co-treatment of EGCG and IFN-β antibody could significantly increase the expression of NP protein and mRNA in the infected cells(P<0.05). CONCLUSION EGCG can induce the production of IFN-β in BEAS-2B by up-regulating the phosphorylation level of p38 signal factor, thereby inhibiting H1N1 replication.