Dihydrolycorine Attenuates Cardiac Fibrosis and Dysfunction by Downregulating Runx1 following Myocardial Infarction

Figure 5

Dihydrolycorine rescued fibrosis and apoptosis in hypoxia-treated cardiomyocytes and induced decreased Runx1 expression. (a) Hypoxia-treated cardiomyocytes were treated with 1.0, 5.0, or 10 μM dihydrolycorine for 24 h, followed by DNA quantification to measure cell number/cell proliferation. (b, c) Relative protein expression of collagen I, TGFβ, smad3, p-smad3, Bax, and Bcl-2 according to western blotting. (d, e) Relative protein expression of Runx1 according to western blotting. (f) Immunofluorescence staining of connexin 43 (red, magnification ×400).  μm. (g) Bar graphs of fluorescence intensity of connexin 43. (h) Immunofluorescence staining of α-SMA (green, magnification ×400).  μm. ^# vs. normoxia and vs. hypoxia; experiments were repeated more than three times.

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