Objective: To observe abnormal immune injury and expressions of high mobility group Box-1 protein(HMGB1) and receptor of advanced glycation end-product(RAGE) in rat pulmonary fibrosis

and the regulatory effect of Buyang Huanwu Tang on HMGB1-RAGE signaling pathway. Method: A total of 144 SD rats were randomly divided into six groups

namely the normal group

the bleomycin (BLM) group

the low

middle and high-dose Buyang Huanwu Tang groups (6.83

13.66

27.32 g·kg-1) and the positive drug group (prednisone

4.2 mg·kg-1). In the animal experiment

the bleomycin trachea injection method was used to reproduce the pulmonary fibrosis animal model

and given high

medium and low-dose Buyang Huanwu Tang by gavage. Samples were extracted on the 7th

14th

28th days after modeling.Reverse transcription PCR(RT-PCR) method was adopted to detect the mRNA expressions of HMGB1 and RAGE in lung tissues

and Western blot method was used to detect the protein expressions of HMGB1 and alpha-smooth muscle action(α-SMA). In the cell experiment

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.Western blot method was used to detect the expression of α-SMA protein. Result: Compared with the blank control group

the mRNA expression of HMGB1 in the BLM model group was obviously up-regulated on the 28th day (P<0.01)

the mRNA expression of RAGE was visibly up-regulated on the 7th and the 14th days (P<0.01)

and the protein expressions of HMGB1 and α-SMA was significantly up-regulated at all times points (P<0.01) in animal experiments. Compared with the BLM model group

in the high-dose Buyang Huanwu Tang group

the mRNA expression of HMGB1 was significantly decreased on the 14th and 28th days (P<0.01)

the mRNA expression of RAGE was significantly down-regulated on the 7th and the 14th days (P<0.01)

and the protein expressions of HMGB1 and α-SMA was clearly down-regulated on all time points (P<0.01) in animal experiments. Compared with blank control group

the 20% serum added HMGB1 group showed a significant rise in the protein expression of α-SMA (P<0.01). Compared with the 20% serum added with HMGB1 control group

different concentrations of Buyang Huanwu Tang-containing serum significantly reduced the protein expression of α-SMA (P<0.01) in the cell experiment. Conclusion: Buyang Huanwu Tang can inhibit the expressions of RAGE and alpha SMA caused by HMGB1 in the rat lung tissues. The results suggest that Buyang Huanwu Tang may prevent and treat pulmonary fibrosis by blocking HMGB1/RAGE signaling pathways and reducing the growth of myofibroblasts.