Objective:To investigate the FSP1mRNA

TGF-βmRNA and HGFmrNA expressinn of lung fibroblasts being affected by alveolar typeⅡcells in pingyangmycin-induced pulmonary fibrosis in rats and its possible mechanism. Methods: Twenty-eight SD rats were randomly divided into two groups as the Pingyangmycin group and saline group. Pulmonary fibrosis was induced by intralracheal instillation with pingyangmycin in the Pingyangmycin group

and the saline group was treated with normal saline

Then ten rats in Pingyangmvcin group and four rats in saline group were sacrificed respectively at the 7th

28th day after intratracheal instillation. Three sacrificed rats in the Pingyangmyein group and three sacrificed rats in the saline group were abstracted alveolar typeⅡcells. The six sacrificed rats in the Pingyangmycin group were abstracted lung fihroblasts. When the two kinds of cells were at the good stale

the experiment group:put the supernate fluid of alveolar typeⅡcells of Pingyangmycin group into the lung fihroblasts of Pingyangmycin group;the control group: put the supernate fluid of alveolar typeⅡcells of saline group into the lung fibroblasts of Pingyangmycin group

then coculture 48 hours

the levels of FSP1mRNA

TGF-βmRNA

HGFmRNA of lung fibroblasts were detected by demi-quantitate RT-PCR. The rest rats of Pingyangmycin grnup and the saline group were used HE stained. Results:(1)The expression of FSP1mRNA

TGF-βmRNA

HGFmRNA in experiment group were higher than the control group at the 7 th

28th day (P<0.01). (2)The levels of FSP1mRNA

TGF-βmRNA in experiment group were not significantly difference between at the 7 th

28th day (P>0.05)

except the level of HGFmRNA in experiment group at the 28th was higher than at the 7th (P<0.01). Conclusion: Alveolar typeⅡcells in pingyangmycin-induced pulmonary fibrosis in rats can promote the FSP1mRNA

TGF-βmRNA expression of lung fibroblasts

and can enhance the procession of pulmonary fibrosis.