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. 2013 Feb 12;136(4):1274–1287. doi: 10.1093/brain/awt002

Figure 1.

Figure 1

Pioglitazone provides vasoprotection in vitro and in vivo. (A and B) Mouse cerebral vascular endothelial cells were treated with pioglitazone (Piog) at different doses with or without infection of an adenovirus carrying PPARγ, small-hairpin PPARγ (shPPARγ) or GFP for 48 h, and then subjected to 16 h oxygen–glucose deprivation (OGD) exposure. Cell viability was determined by MTT assays (A) and the lactate dehydrogenase method (B). Pioglitazone significantly reduced oxygen–glucose deprivation-induced cerebral vascular endothelial cell death in a dose-dependent manner. Gain of PPARγ function by infection of an adenovirus (Ad) carrying PPARγ in cerebral vascular endothelial cells potentiated pioglitazone-mediated cytoprotection after 16 h of oxygen–glucose deprivation exposure, whereas loss of PPARγ function by adenovirus-mediated PPARγ RNA interference reversed this effect. (C) Mice were treated with pioglitazone (intraperitoneally 2 mg/kg) at the start of 24 h of middle cerebral artery reperfusion after 1 h of middle cerebral artery occlusion (n = 6). Cerebrovascular permeability was determined by Evans blue extravasation. Pioglitazone significantly attenuated ischaemia-triggered increases in cerebrovascular permeability. Data are expressed as mean ± SEM. *P < 0.05 versus oxygen–glucose deprivation or Sham group. #P < 0.05 versus oxygen–glucose deprivation + pioglitazone + Ad.GFP; ##P < 0.05 versus ischemia + vehicle (Isch + Veh) group.