Fig. 1: Ischemic postconditioning prevents VDAC decline in rat hippocampal CA1 subfield.

a and b Immunoblots and quantification of VDACs and COX4 after ischemia and reperfusion (I/R) without or with ischemic postconditioning in the hippocampal CA1 subfield (a) and in the resistant CA3/DG subfield (b) (n = 3 rats per group); relative levels of VDACs and COX4 were normalized to respective sham groups. Actin was used as a loading control. Data are shown as the mean ± SD of three independent experiments. *P < 0.05 versus the sham group; n.s., not significant; One-way ANOVA. ^#P < 0.05 versus ischemic postconditioning, unpaired t-test. c Quantificational analysis of mtDNA copy number in the hippocampal CA1 subfield after I/R (n = 3 rats per group); Relative mtDNA copy number was normalized to sham groups. Data are shown as the mean ± SD of three independent experiments. n.s., not significant; one-way ANOVA