Rosiglitazone Restores Endothelial Dysfunction in a Rat Model of Metabolic Syndrome through PPARγ- and PPARδ-Dependent Phosphorylation of Akt and eNOS

Figure 2

Rosiglitazone attenuated the vascular dysfunction in rats on HFD through PPARγ and PPARδ activation. (a, b) Acetylcholine- (a) and nitroglycerin- (b) induced relaxation in isolated mesenteric arteries from rats on normal chow diet and HFD diet. (c, d) Effects of rosiglitazone pretreatment on the Acetylcholine-induced vasorelaxation in rats on HFD in the absence or presence of L-NAME (c) or PPAR antagonists (d). RGZ: rosiglitazone; L-NAME: eNOS inhibitor; GSK0660: PPARδ antagonist; GW9662: PPARγ antagonist; GW6471: PPARα antagonist. Data are means ± s.e.m. from 6 separate experiments. *𝑃<0.05, **𝑃<0.01 between the E_max of indicated groups.

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