Fig 3.

Delayed PFT-α treatment promotes the proliferation of NPCs and inhibits apoptosis in the SVZ in stroke rats. (A). Rats received PFT-α or vehicle from days 6 to 9 after MCAo. BrdU was administered daily for 3 days after PFT-α injection. (B) PFT-α treatment increased the density of BrdU immunoreactivity (optical density) in SVZ (Δ, p<0.05, 2-way ANOVA). The increase in BrdU labeling was more prominent in the anterior SVZ (* p<0.05, post-hoc Newman-Keuls test, 2-way ANOVA). (C) Representative photomicrographs of the anterior SVZ indicate that BrdU labeling was enhanced in the stroke animals treated with PFT-α. Calibration = 100 μm. (D). Representative photomicrographs of the anterior subependymal zone indicate that density of PCNA positive cell increased in the stroke animals treated with PFT-α. (Panels 2 and 4, from the far left) compared to vehicle-treated animals (Panels 1 and 3) on day 10 after MCAo. Panels 3 and 4 are images at higher magnification. Scale bar = 50 μm. (E) PFT-α significantly enhanced the number of PCNA positive cells at the anterior portion of the subependymal zone (*p<0.05, t test). (F) Delayed PFT-α treatment significantly suppressed TUNEL labeling in the SVZ on day 10 after MCAo (Δ, p<0.05, 2-Way ANOVA). (G) PFT-α suppresses the expression of PUMA. SVZ tissues were harvested from PFT-α or vehicle treated stroke rats on the 4th day of PFT-α treatment. p53-regulated genes (mRNA levels) were determined by qRT-PCR. All the genes were normalized to the housekeeping gene PGK1 mRNA level. PFT-α did not change the level of Bcl2 or Bax genes. However, it decreased the mRNA levels of PUMA (*p<0.05, t test).