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

Figure 4

Rosiglitazone increased NO production in cultured endothelial cells through PPARγ- and PPARδ-dependent PI3K/Akt pathway. (a) Representative images of DAF-2 DA-loaded cells treated with rosiglitazone (RGZ) in the presence or absence of PPAR antagonists or LY294002, the PI3K inhibitor. (b) Summary data of the DAF-2 fluorescence. Data are means ± SEM from 4 separate experiments. **𝑃<0.01 versus Control. ^##𝑃<0.01 versus RGZ.

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