Objective To explore the mechanism of Yinhua Pinggan Keli（ 银花平感颗粒） in anti influenza A/PR8/34（ H1N1） virus in vitro. Methods MTT method was used to detecte maximum non-toxic concentration of drugs against macrophages（ TC

0

）

median toxic concentration against cells( TC

50

) and antiviral efficiency of different drug administration methods. Half inhibited concentration( IC

50

) and treatment index（ TI） in virus infection were calculated by probit regression analysis. RAW264. 7 cells infected by influenza H1 N1 virus were intervened by ribavirin（ 62. 5 μg/ml）

Yinhua Pinggan Keli of high（ 500 μg/ml）

medium（ 250 μg/ml） and low（ 125 μg/ml）dose. After 4

16 and 24 hours

the cells were collected. Changes of Toll-like receptor 7（ TLR7）

myeloid differentiation factor 88（ My D88）

nuclear factor p65（ NF-κB p65）

interferon regulatory factor 7（ IRF7） of cells in all groups were examined by real time fluorescent quantitative polymerase chain reaction（ PCR） method. Results Yinhua Pinggan Keli of 31. 25 to 500 μg/ml might reduce influenza virus replication. The antiviral effective rate in the medication group was the highest among all groups after administration for 24 h. Compared with the normal control group at the same time point

the expressions of TLR7

My D88

IRF7 and NF-κB p65 mRNA in the model control group increased

with peak at 16 h. The difference was significant compared with 4 h and 24 h in the same group（ P

<

0. 05 or P

<

0. 01）. After medicine intervention

the expression levels of TLR7

My D88

IRF7 and NF-κB p65 mRNA induced by influenza virus for 4

16 and 24 h were down-regulated in the Yinhua Pinggan Keli high

medium dose groups and the ribavirin group（ P

<

0. 05 or P

<

0. 01）. Especially

the down-regulation effect on the expressions of TLR7

My D88 and NF-κB p65 mRNA in the Yinhua Pinggan Keli high dose group was superior to that in the ribavirin group. Conclusion Yinhua Pinggan Keli in vitro might inhibit influenza virus replication. The anti-virus effect was mainly by therapeutic medication

which might relate to inhibiting TLR7/My D88/IRF7 signaling pathway and activation of NF-κB p65. The treatment effect on influenza of high dose was superior to ribavirin.