Vigilancia Tecnológica

BBR treatment inhibited THBS2 expression to inactivate the Smad2/3 pathway, consequently inhibiting pulmonary fibrosis by repressing the proliferation, migration, invasion, inflammation, and oxidative stress of human lung fibroblast?like cells.ABSTRACTPulmonary fibrosis (PF) is a progressive and irreversible lung disease. Previous studies have shown that berberine (BBR) ameliorates PF; however, the mechanism of BBR regulating PF remains unclear. mRNA expression of thrombospondin 2 (THBS2) was analyzed by quantitative real?time polymerase chain reaction. Protein expression level was detected by western blotting assay or immunohistochemistry assay. Cell function was analyzed using cell counting kit?8 assay, 5Ethynyl?2'?deoxyuridine assay, transwell invasion assay, wound?healing assay, enzyme?linked immunosorbent assays, and colorimetric assay. PF mouse model was established using bleomycin (BLM) to analyze the effect of BBR on PF. The results showed that THBS2 expression was upregulated in the lung tissues of BLM?induced PF mice and transforming growth factor??1 (TGF??1)?induced HLF cells. BBR ameliorated BLM?induced PF in vivo. TGF??1 treatment induced HLF cell proliferation, invasion, migration, inflammation response, and oxidative stress, accompanied by increases in collagen I, fibronectin, and ??SMA protein expression; however, these effects were attenuated after THBS2 silencing. In addition, BBR attenuated TGF??1?induced pro?fibrotic phenotypes of HLF cells and BLM?induced PF through the inactivation of the THBS2/Smad2/3 pathway. Thus, BBR inhibited BLM?induced PF by inactivating the THBS2/Smad2/3 pathway, providing a theoretical basis for PF treatment with BBR.