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Effect of rutin on TGF-β1 induced fibrosis of cardiac fibroblasts
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DOI   10.11656/j.issn.1672-1519.2025.01.14
Key Words   rutin;cardiac fibrosis;cardiac fibroblasts;TGF-β1/Smad signaling pathway
Author NameAffiliationE-mail
ZHANG Guannan School of Life Sciences, Ningxia University, Yinchuan 750021, China  
NIU Pilian School of Life Sciences, Ningxia University, Yinchuan 750021, China  
JING Ruixin School of Life Sciences, Ningxia University, Yinchuan 750021, China  
SHI Xinwei Shanxi Institute of Botany, Xi'an 710061, China  
BAI Mingsheng School of Life Sciences, Ningxia University, Yinchuan 750021, China baimingsheng@163.com 
Abstract
    [Objective] To explore the effect of rutin on transforming growth factor-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 μmol/L captopril and cells) and administration group(10 ng/mL TGF-β1+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-β1/Smad pathway-related proteins were detected by Western blot. The gene expression levels of Acta 2,Vim,FN,Col Ⅰ1a1,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,CollageⅠ,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 of α-SMA in the TGF-β1 model group was significantly enhanced. Compared with the model group,the green fluorescence intensity of α-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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