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Fig. 4 | Cardiovascular Diabetology

Fig. 4

From: Repressive H3K27me3 drives hyperglycemia-induced oxidative and inflammatory transcriptional programs in human endothelium

Fig. 4

GSK126 recovers high glucose-induced endothelial dysfunction. A Endothelium-dependent relaxations to acetylcholine (Ach) and endothelium-independent relaxations to sodium nitroprusside (SNP) in mouse aortic rings after exposure to normal (5 mmol/l) and high (25 mmol/l) glucose in the presence and in the absence of GSK126 (5 µmol/l; n = 4–6/group). B Representative confocal images and quantification of H3K27me3, EZH2, SOD1, and SOD2 protein expression in aortas from WT, db/db mice, and db/db mice exposed to vehicle or GSK126 (5 µmol/l; n = 6/group). Scale bar = 500 μm

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