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

Figure 3

Rosiglitazone increased the phosphorylation of Akt and eNOS through PPARγ and PPARδ activation in cultured endothelial cells. (a) Representative immunoblots of phosphorylated and total eNOS and Akt in cells treated with rosiglitazone (RGZ) in the presence or absence of PPAR antagonists. GAPDH was used as loading control. (b, c) Summary densitometry data showing the ratio of phospho-eNOS (p-eNOS) relative to total eNOS (eNOS) and phospho-Akt (p-Akt) relative to total Akt (Akt). Data are means ± SEM from 3 separate experiments. *𝑃<0.05, **𝑃<0.01 versus Control. ^#𝑃<0.05 versus RGZ.

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