Myricetin Possesses Potential Protective Effects on Diabetic Cardiomyopathy through Inhibiting IκBα/NFκB and Enhancing Nrf2/HO-1

Figure 2

Myricetin inhibited the cardiac fibrosis of DCM induced by treatment of STZ. (a) Histological sections of mouse hearts stained by picrosirius red (PSR) for fibrosis and immunohistochemistry for collagen I/III (). (b) The calculation of PSR positive area. (c) and (d) The calculation of collagen I/III positive area (). (e) and (f) The relative expression of biomarkers of cardiac fibrosis, fibronectin (Fn), and connective tissue growth factor (CTGF) (). (g) Representative blots of transforming growth factor (TGFβ1), T-Smad3, p-Smad3, and glyceraldehyde-3-phoshate dehydrogenase (GAPDH), (). (h) and (i) Histogram indicated the expression changes among different groups (). as compared with the corresponding CON or M group. ^# as compared with STZ group, GAPDH was selected as the internal reference, and all of the proteins were normalized to GAPDH before quantitative statistics.

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