Effect of rutin on TGF-β1 induced fibrosis of cardiac fibroblasts
[Objective]To explore the effect of rutin on transforming growth fact or-β1(TGF-β1)-induced fibrosis of cardiac fibroblasts(CFs)and the TGF-β1/Smad signaling pathway.[Methods]The CFs cell model induced by TGF-β1 was constructed,and the groups were set as follows:control group(complete medium+cells),model group(containing 10 ng/mL TGF-β1+cells),positive control group(10 ng/mL TGF-β1+10 pimol/L captopril and cells)and administration group(10 ng/mL TGF-[31+200 µg/mL rutin and cells).The expression of α-smooth muscle actin(α-SMA),Vimentin(Vim),Fibronectin(FN),Collagen I,Collagen Ⅲ and TGF-[31/Smad pathway-related proteins were detected by Western blot.The gene expression levels of Acta 2,Vim,FN,Col Ⅰ 1a1,matrix metalloproteinase 2(MMP-2)and matrix metalloproteinase 9(MMP-9)were detected by quantitative real-time polymerase chain reaction(qPCR).Immunofluorescence was used to detect the expression and localization of the key protein α-SMA to explore the effect of rutin on TGF-β1-induced CFs fibrosis.[Results]After CFs were induced by TGF-β1,the expression of Vim,FN,Collage Ⅰ,Collage Ⅲ,TGF-β1/Smad signaling pathway-related proteins was successfully activated.After intervention with 200 µg/mL rutin,the activation of Vim,FN,Collage Ⅰ,Collage Ⅲ,TGF-β1/Smad signaling pathway-related proteins and mRNA was inhibited,thereby alleviating the occurrence of myocardial fibrosis.The results of immunofluorescence assay showed that compared with the control group,the green fluorescence intensity ofα-SMA in the TGF-[31 model group was significantly enhanced.Compared with the model group,the green fluorescence intensity ofα-SMA was significantly weakened in the 200 μg/mL rutin group.[Conclusion]The results of this study showed that 200 μg/mL rutin alleviated myocardial fibrosis by inhibiting the expression of Vim,FN,Collage Ⅰ,Collage Ⅲ,α-SMA and TGF-β1/Smad signaling pathway-related proteins and mRNA induced by TGF-β1.
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