Objective To investigate the role of ginkgo biloba extract (GBE) in TGFβ1-induced myocardial fibroblast proliferation of neonatal rats and its mechanism,and explore the role of miR-133a in myocardial fibroblast proliferation. Methods TGFβ1 was used to induce myocardial fibroblast proliferation of neonatal rats to establish cell proliferation model. GBE was added to the above cell proliferation model. CCK8 assay and flow cytometry were applied to detect cell proliferation and cell cycle,respectively. Mimic and siRNA were used to construct a model for overexpression and inhibition of miR-133a,respectively. RT-PCR was used to detect the expressions of miR-133a,TGFβ1,and TGFβ receptor. Results TGFβ1 promoted the viability of myocardial fibroblasts and increased the proportion of myocardial fibroblasts entering S phase from G0/G1 phase,while GBE significantly antagonized the TGFβ1-induced effects. In TGFβ1-induced myocardial fibroblast model,GBE treatment or overexpression of miR-133 a significantly inhibited TGFβ1-induced myocardial fibroblast proliferation and mRNA expression of TGFβ receptor,while inhibiting miR-133a expression in the cell model partially counteracted the regulatory effect of GBE on cell proliferation. Conclusion GBE may remarkably improve myocardial fibroblast proliferation induced by TGFβ1 . It may be attributed to the upregulation of miR-133a and inhibition of TGFβ receptor expression by GBE.
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