[Effect of salvianolic acid B on proliferation and apoptosis of human nasal polyps fibroblasts].

Abstract

Objective:The aim of this study is to discuss the effects and mechanism of salvianolic acid B (SAB) on the proliferation and apoptosis of human nasal polyps fibroblasts (NPFs). Method:The NPFs were treated with SAB at different concentrations (5, 10, 20, 40 μmol/L). CCK-8 assay was used to determine the inhibition of SAB on the proliferation of NPFs and determined the optimum concentration for the following experiments. The NPFs were divided into four groups: a) control group: the cells were cultured in DMEM without TGF-β1 or salvianolic acid B; b) the TGF-β1 group: the cells were cultured in DMEM containing 5 ng/ml TGF-β1; c) the SAB group: the cells were cultured in DMEM containing SAB at the optimum concentration by CCK-8 assay; d) the TGF-β1+SAB treatment groups: the cells were cultured in DMEM containing 5 ng/ml TGF-β1 and SAB at the optimum concentration by CCK-8 assay. MTT assay was used to determine the proliferation of NPFs in four groups. The apoptosis rate was analyzed by Annexin-V FITC/PI double staining. The activities of Caspase-3 were detected with spectrophotometric method. Apoptosis related proteins Bcl-2 and Bax were measured by western blot. Result:CCK-8 assay showed that SAB could inhibite NPFs proliferation in a dose-dependent pattern (P<0.05). The following experiments were carried out with the concentration of salvianolic acid B at 10 μmol/L. MTT results showed that SAB could inhibit the proliferation of NPFs stimulated by TGF-β1 (P<0.01). Annexin-V FITC/PI double staining showed that SAB could induce apoptosis of NPFs (P<0.05). The activities of Caspase-3 were increased with SAB (P<0.05). Western blot results showed that SAB reduced the Bcl-2 protein expression, and increased the Bax protein expression and the ratio of Bax/Bcl-2 (P<0.05). Conclusion:Salvianolic acid B could inhibit proliferation and induce apoptosis of NPFs. Its mechanism may be associated with increasing the activities of Caspase-3 by inhibiting the expression of Bcl-2 protein and promoting the expression of Bax protein.