Polydatin Protects Diabetic Heart against Ischemia-Reperfusion Injury via Notch1/Hes1-Mediated Activation of Pten/Akt Signaling

Figure 3

Effect of polydatin and DAPT on cardiac function in MI/R-injured diabetic rats. The diabetic animals received MI/R operation in the presence or absence of polydatin or DAPT treatment. TUNEL staining and Evans blue-TTC double staining were performed after 6 hours of reperfusion. Cleaved caspase-3 expression, caspase-3 activity, and plasma CK and LDH activity measurement were performed after 3 hours of reperfusion. (a) Representative photomicrographs of in situ detection of apoptotic myocytes by TUNEL staining (×200, bar = 200 μm). Apoptotic nuclei were stained with TUNEL (row 1, green staining). Total nuclei were stained with DAPI (row 2, blue staining). Cardiomyocytes were stained with anti-α-sarcomeric actin (row 3, red staining). (b) Bar diagram showing apoptotic index (percentage of TUNEL-positive nuclei). (c) Bar diagram showing cleaved caspase-3 expression. Top images: representative blots. (d) Bar diagram showing caspase-3 activity. (e) Bar diagram showing myocardial infarct size. Top images: representative photographs of heart sections. Blue-stained area indicates nonischemic, normal region; red-stained area, ischemia-reperfused but not infarcted region; and negative-stained area, ischemia-reperfused infarcted region. (f) and (g) Bar diagram showing plasma CK and LDH activity. The results are expressed as the mean ± SEM. samples per group. / versus the sham group, / versus the MI/R + V group, and versus the MI/R + PD group. MI/R, myocardial ischemia-reperfusion; V, vehicle; PD, polydatin; AAR, area at risk; INF, infarct area; CK, creatine kinase; LDH, lactate dehydrogenase.

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