Objective:To observe the effect of maackiain(MA)on the proliferation and activation of cardiac fibroblasts induced by transforming growth factor β(TGFβ)and explore the role of AMPK/SIRT3 pathway.Methods:Rat cardiac fibroblasts were randomly divided into the control group,MA group,TGFβ group,and TGFβ+MA group.After 24 hours of culture,the CCK-8 method was used to de-tect the inhibitory effect of different concentrations of maackiain on fibroblast proliferation;RT-PCR was used to detect transcript levels of α-smooth muscle actin(α-SMA)and connective tissue growth fac-tor(CTGF);cell immunofluorescence staining was used to detect α-SMA and phosphorylated histone H3(pH3);Western Blot was used to detect the expression of α-SMA,CTGF,adenylate activated pro-tein kinase(AMPK),p-AMPK and SIRT3.Results:CCK-8 cell viability test and pH3 staining results showed that maackiain could significantly inhibit the proliferation of fibroblasts;the fibrosis-related fac-tors expressions of α-SMA and CTGF in the TGFβ group were higher than those in the control group,while treatment of MA could inhibit the expression of fibrosis-related factors.In terms of mechanism,Western Blot showed that MA could activate the AMPK/SIRT3 signaling pathway,and Compound C(CC),an AMPK inhibitor,could eliminate the anti-fibrosis effect of MA and activate the AMPK/SIRT3 pathway.Conclusion:MA acts on rat cardiac fibroblasts and inhibits TGFβ by activating the AMPK/SIRT3 pathway-induced proliferation and activation of cardiac fibroblasts.
MaackiainMyocardial FibrosisCardiac FibroblastAMPK/SIRT3 Signal Pathway
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