Bursopentin Reduce HLF ECM By Mediating TGF-β1/Smad Signaling Pathway

[Objective]:To investigate the effects of Bursopentin on expressions of extracellular matrix in human lung fibroblasts and by mediating TGF-β1/Smad signal pathway.[Method]:HLF were cultured in vitro and divided into five groups,A control group: the cells were cultured in DMEM without TGF-β1or Bursopentin;a TGB-β1treatment group:the cells were cultured in DMEM containing5μg/L TGF-β1; three TGF-β1+Bursopentin treatment groups:the cells were cultured in DMEM containing5μg/L TGF-β1and at the same time intervened with BP5at different concentrations(2.5ug/ml,5ug/ml,10ug/ml respectively).Expression of a-SMA was performed using a fluorescent2strategy labeling; Collagen-I, p-Smad2/3, p-Smad3, Smad7proteins were measured by Western blot.[Result]:TGF-β1stimulated group showed positive expression of a-SMA, implying TGF-β1had induced fibroblasts to differentiate into myofibroblasts. In TGF-β1stimulated group,and the expression levels of collagen-Ⅰ proteins significantly increased.Meanwhile, the expression levels of p-Smad2/3and p-Smad3proteins increased with statistical significance (P<0.01), but the expression level of Smad7protein reduced (P<0.05)。 But in the TGF-β1+BP5group overexpressions of collagen-Ⅰ, α-SMA, p-Smad2and p-Smad3induced by TGF-β1were obviously inhibited by BP5,especially at the BP5concentrate of10μg/ml;Otherwise, the up-regulation of Smad7was found.[Conclusions]:Bursopentin can reduce the expressions of collagen-I and α-SMA protein from fibroblast stimulated by TGF-β1,maybe through inhibiting TGF-β1/Smads transduction pathway. It is suggested that Bursopentin may have intervention in pulmonary fibrosis.