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. 2017 Apr 4;7:45827. doi: 10.1038/srep45827

Figure 5. Glycated PON1 via ER stress induces endothelial dysfunction in rats.

Figure 5

(A–D) SD rats were injected with native or glycated PON1 (1 mg/kg/day) for 7 consecutive days via tail vein. Aortas from rats were cut into rings and were mounted in organ chamber to detect vessel bioactivity. Endothelium-dependent relaxation of the aortic rings in response to Ach in (A), Endothelium-independent relaxation of the aortic rings in response to SNP in (B), ROS productions in (C), and the levels of p-PERK, p-eIF2α, ATF6 and CHOP in (D) were assayed. 10–15 rats in each group. *P < 0.05 vs. Control rats. (E,F) SD rats were administrated with tempol (1 mM in the drinking water), 4-PBA (1 g/kg/day), and BAPTA (5 mg/kg per day) for 2 weeks followed by injection of glycated PON1 (1 mg/kg/day, 7 consecutive days) via tail vein. Aortas from rats were cut into rings and were mounted in organ chamber to detect vessel bioactivity. The relaxation was induced by Ach in (D) or SNP in (E). Each data point represents relaxation expressed as a percentage of the value obtained for PE-preconstricted aorta. Two aortic rings were isolated from each rat. 10–15 rats in each group. *P < 0.05 vs Gly-PON1 alone. The presented blots were cropped from the full blots shown in Supplementary Figure S11.