Inhibition of adenine nucleotide translocator pore function and protection against apoptosis in vivo by an HIV protease inhibitor
J. Clin. Invest. Joel G.R. Weaver, et al. 115:1828 doi:10.1172/JCI22954 [Go to this article.]

Figure 2
Effects of NFV/RIT on infarct size, neuronal loss, and behavioral impairment following 1 hour of MCAO and 24 hours of reperfusion. (A) Schematic representation of coronal forebrain sections were analyzed. Infarcted and control hemispheres are indicated. DE, diencephalon. The tissue areas analyzed by TTC as shown in B are indicated in blue. The areas analyzed for NeuN and TUNEL reactivity as shown in D and E are indicated in orange. (B) Mice pretreated with NFV/RIT exhibit a smaller infarct 24 hours after surgery, as assessed by TTC staining, relative to mice pretreated with vehicle or control (sham) mice (*P < 0.05, Student’s t test). Open circles, no pretreatment; filled circles, vehicle pretreatment; filled squares, NFV/RIT pretreatment. (C) NFV/RIT protects neurons from apoptotic-like death. (D) Quantitation of overall neuronal loss following MCAO or sham surgery. Both vehicle- and NFV/RIT-treated animals exhibit a comparable reduction in neuronal number following MCAO (^#P = 0.08, *P < 0.05, ANOVA, post-hoc Dunnett t test). (E) NFV/RIT-treated animals are protected from apoptotic-like death following MCAO surgery. The majority of remaining NeuN-positive cells in vehicle-treated mice are apoptotic, while TUNEL reactivity is significantly reduced in NFV/RIT-treated animals (**P < 0.01, ANOVA, post-hoc Dunnett t test). (F) NFV/RIT improves neurological recovery following MCAO. Animals tested immediately after MCAO surgery (0.5 hours) show equivalent motor deficits. After 24 hours of reperfusion, NFV/RIT exhibit significant behavioral improvement relative to 0.5 hours or vehicle-treated cells. *P < 0.05; **P < 0.01, ANOVA, post-hoc Tukey test. Data represent mean ± SEM.