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. 2015 May 21;3(4):537–542. doi: 10.3892/br.2015.465

Figure 3.

Figure 3.

Rosiglitazone inhibits MCT-induced pulmonary arterial hypertension in rats by regulating the PTEN/PI3K/Akt signaling pathway. (A) MCT increased Akt serine-473 phosphorylation (p-Akt) as the fold-change increases when normalized to the total Akt expression, while these effects were blocked by rosiglitazone. Data represent mean ± standard error of the mean (SEM) (n=3 in each group). (B) Western blotting of PTEN and GAPDH in the control, MCT and MCT + Rosi groups. The results show a significant decrease in PTEN expression after administration of a single dose of MCT (60 mg/kg), which was ameliorated by treatment with rosiglitazone (5 mg/kg/day) for 4 weeks. Input GAPDH served as a loading control, data represent mean ± SEM. *P<0.05 vs. control; #P<0.05 vs. MCT-treated group; n=3 for each group). Rosi, rosiglitazone; PTEN, phosphatase and tensin homologue deleted on chromosome ten; Con, control; MCT, monocrotaline; PI3K, phosphatidylinositol 3-kinase.