p53 Inhibition Protects against Neuronal Ischemia/Reperfusion Injury by the p53/PRAS40/mTOR Pathway

Figure 2

Neurological deficits, infarction size, and neuronal apoptosis were less severe 48 h after MCAO in p53 KO rats. (a) The neurological deficit scores were significantly lower in p53^-/- mice 48 hrs after MCAO. Compared with WT mice, the neurological deficit scores were lower in p53^+/- mice and much lower in p53^-/- mice. vs. WT+sham; ^# vs. WT+MCAO. -8/group. (b) The infarction size normalized to the bilateral cortex was smaller in p53^-/- and p53^+/- mice than in p53^+/+ mice 48 h after MCAO. vs. the p53^+/++sham group; ^# vs. the p53^+/++MCAO group. (c) The analyzed samples were obtained from ischemic brains of mice 48 h after MCAO. After HE staining (×100), more normal neurons were observed in p53 KO and heterozygous mice than in p53 WT mice, which suggested less severe cerebral I/R injury. (d) By performing TUNEL staining in the ischemic brains of mice after MCAO (×400), positive apoptotic cell counts (red) were quantified. The number of positive TUNEL cells was significantly lower in p53^+/- and p53^-/- mice than in p53^+/+ mice. vs. the p53^+/++sham group; ^# vs. the p53^+/++MCAO group. –8/group.

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