Fig. 6: The decrease of VDACs results from elevated miR-7 after ischemia and reperfusion.

a qReal-time PCR analysis of miR-7 levels in the hippocampal CA1 subfield and in the resistant CA3/DG subfield from rats subjected to global ischemia followed by reperfusion (I/R) without or with postconditioning (n = 6 rats per group in CA1 subfield; n = 5 rats per group in CA3/DG subfield). Relative levels were normalized to respective sham groups. Data are the mean ± SD. *P < 0.05 versus the sham group; n.s., not significant; one-way ANOVA. b qReal-time PCR analysis of miR-7 levels in CA1 subfield 24 h after I/R. Rats were treated with Anti-7 or NC 50 min after I/R (n = 3 rats per group); Relative levels were normalized to sham groups. Data are the mean ± SD. *P < 0.05 versus the sham group; ^#P < 0.05 versus the I/R group; n.s., not significant; one-way ANOVA. c Immunoblots and quantification of VDACs in the CA1 subfield 24 h after treated with Anti-7 or NC (n = 3 rats per group); Relative levels were normalized to sham groups. Actin was used as a loading control. Data represent the mean ± SD of three independent experiments. *P < 0.05 versus the sham group; ^#P < 0.05 versus the I/R group; n.s., not significant; one-way ANOVA. d Conservative analysis of miR-7 sequence in humans, rats, mice, and zebrafish. e qReal-time PCR analysis of miR-7 in peripheral venous blood collected within 24 h from patients subjected to acute ischemic stroke (AIS) or healthy controls (n = 8 per group). Relative levels were normalized to control groups. Data represent the mean ± SD. *P < 0.05 versus the healthy control group; unpaired t-test with Welch’s correction