Objective: To observe the activation of extracellular regulated protein kinase 1/2(ERK1/2) and nuclear factor kappa B(NF-κB) signaling pathway after stimulating normal lung fibroblasts (HFL1) by high mobility group Box-1 protein (HMGB1)

which can induce immune damage in pulmonary fibrosis

as well as the intervening effect of Buyang Huanwu Tang-containing serum on above signal pathways. Method: The drug-containing serum pharmacological methodology was adopted. Buyang Huanwu Tang-containing serum with concentrations of 5%

10%

15%

20%

and blank serum were adopted to intervene normal lung fibroblasts (HFL1) stimulated by HMGB1.The enzyme-linked immunosorbent assay (ELISA) method was used to detect the expression of interleukin-1β (IL-1β)

and the immune protein imprinting method (Western blot method) was applied to detect total protein expression of ERK1/2 and cell cytoplasm and nucleus protein expression of NF-κB p65. Result: Compared with blank control group

HMGB1 can promote the expressions of IL-1β

ERK1/2

NF-κB p65 in HFL1 cell (P<0.05

P<0.01). Compared with the 20% serum control added with HMGB1 group

the expressions of IL-1β

ERK1/2

NF-κB p65 were increased in HMGB1 stimulation group. Compared with HMGB1 stimulation group

all of Buyang Huanwu Tang-containing serum groups could reduce the expressions of IL-1β

ERK1/2

NF-κB p65.Among them

15% and 20% Buyang Huanwu Tang-containing serum could obviously reduce the expression of ERK1/2(P<0.05); 10% Buyang Huanwu Tang-containing serum in cell cytoplasm

and 20% Buyang Huanwu Tang containing-serum in cell nucleus could clearly decrease the expression of NF-κB p65 (P<0.05); And 15% Buyang Huanwu Tang-containing serum could visibly reduce the expression of IL-1β (P<0.05). Conclusion: In the in vitro experiment

Buyang Huanwu Tang-containing serum can inhibit the activation of ERK1/2-NF-κB signaling pathways caused by HMGB1 in HFL-1

and reduce the secretion of inflammatory factor IL-1β. The results suggest that Buyang Huanwu Tang may prevent and treat pulmonary fibrosis by regulating ERK1/2-NF-κB signaling pathways.