Fig. 7: PRT@PPMP reverses myocardial injury by enhancing glycolysis during hypoxia and improving mitochondrial function during reoxygenation. | Cell Death Discovery

Fig. 7: PRT@PPMP reverses myocardial injury by enhancing glycolysis during hypoxia and improving mitochondrial function during reoxygenation.

From: Upregulation of Hsp27 via further inhibition of histone H2A ubiquitination confers protection against myocardial ischemia/reperfusion injury by promoting glycolysis and enhancing mitochondrial function

Fig. 7

A Scheme of the time axis representing the design of hypoxic cell research. B Immunofluorescence results showing Hsp27 expression in control cardiomyocytes and hypoxic cardiomyocytes treated with PRT, PRT@PPM, and PRT@PPMP. C, D Glycolytic stress analyses of cardiomyocytes using the Seahorse XF analyzer in response to oligomycin, glucose, and 2-DG. E Intracellular ATP levels in cardiomyocytes. Data are presented as mean ± SD (n = 6). #P < 0.05 vs. Control group; *P < 0.05 vs. Hypoxia group. F Scheme of the time axis illustrating the design of H-R-induced cell study. G Representative images of JC-1 fluorescence in the control and reoxygenated cardiomyocytes treated with PRT, PRT@PPM, and PRT@PPMP. H Immunofluorescence detection of cellular ROS levels in cardiomyocytes. I Mitochondrial ROS levels in cardiomyocytes. J MDA levels in cardiomyocytes. K Relative mRNA levels of ptgs2 in cardiomyocytes determined using qRT-PCR. L–M Detection of cardiomyocyte viability. Data are presented as mean ± SD (n = 6). #P < 0.05 vs. Control group; *P < 0.05 vs. Reoxygenation group. Scale bars: (B, H) 50 μm; (G) 25 μm; and (L) 100 μm.

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