To investigate the expression of phosphorylated peroxisome proliferators-activated receptor γ (p-PPARγ) in the aging thoracic aorta of spontaneously hypertensive rat (SHR) and the inhibitory effect of rosiglitazone on the phosphorylation of PPARγ. Methods: 16, 32 and 64 week-old Wistar-Kyoto rats (WKY) and SHR were randomly and respectively divided into WKY, SHR and SHR+rosiglitazone group (9 in each group). The rats in SHR+rosiglitazone group were treated with rosiglitazone (5 mg/kg, intragastrically) for 56 d, whereas normal saline was applied in WKY and SHR groups. Systolic blood pressure (SBP) of rats was measured by tail cuff method. Histopathological damage of thoracic aorta was analyzed using Hematoxylin-Eosin (HE) staining. Immunohistochemical staining and west blot were performed to test the level of p-PPARγ protein in the thoracic aorta arising from each group. Results: The SBP in 16, 32 and 64 week-old SHR were significantly higher as compared with those in matched WKY rats (P<0.05, respectively). HE staining showed increased content of smooth muscle cell, wrinkled lining endothelium and increased thickness of intal elastic lamina in the thoracic aorta of SHR. Immunohistochemical staining and west blot indicated that the levels of p-PPARγ in the thoracic aorta arising from SHR were obviously higher than those in the thoracic aorta arising from WKY rats (P<0.05, respectively). Importantly, the high SBP, histopathological abnormalities of the thoracic aorta and elevated p-PPARγ expression were prominently abrogated by rosiglitazone treatment in SHR (P<0.05, respectively). Furthermore, the SBP, histopathological abnormalities of the thoracic aorta and p-PPARγexpression were positively correlated with age in SHR (P<0.05, respectively). Conclusions: The PPARγ phosphorylation was observed in the thoracic aorta of SHR and its expression was increased by the increase of age. Furthermore, rosiglitazone inhibited the PPARγ phosphorylation and suppressed vascular aging in SHR.