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

Figure 6

(a–e) Dihydrolycorine mitigated adverse cardiac remodeling after myocardial infarction (MI) reducing Runx1 in vivo and in vitro. Ad-EV, Ad-Runx1, and Ad-sh-Runx1 (10 mL/mL, MOI: 100 : 1) were transfected into experimental cardiomyocytes for 6-8 hours, and these cells were treated with or without dihydrolycorine (15 μM) under hypoxia conditions. MI rats () and sham rats () were injected with Ad-EV, Ad-Runx1, and Ad-sh-Runx1 (10 mL at each of four sites, PFU/mL) into the left ventricle free wall and then treated with or without dihydrolycorine (20 mg/kg). (a, b) Relative protein expression of collagen I, TGFβ, smad3, p-smad3, Bax, and Bcl-2 according to western blotting. (c) Immunofluorescence staining of connexin 43 (red, magnification ×400).  μm. (d) Bar graphs of fluorescence intensity of connexin 43. (e) Immunofluorescence staining of α-SMA (green, magnification ×400).  μm. (f–i) (f, g) Relative protein expression of collagen I, TGFβ, smad3, p-smad3, Bax, and Bcl-2 according to western blotting. (h) Cardiac myocyte hypertrophy was evaluated using WGA (magnification ×100) staining of left ventricular tissue from rats.  μm. (i) Myocardial fibers in myocardial tissue sections were stained with hematoxylin and eosin (H&E, magnification ×40).  μm. ^# vs. normoxia and vs. hypoxia; or ^# vs. sham and vs. MI; experiments were repeated more than three times.

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