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. 2020 Sep 2;10:14435. doi: 10.1038/s41598-020-71326-x

Figure 5.

Figure 5

CsA-NP reduced infarct size after cerebral IR injury by blocking mPTP opening and Pitava-NP reduced infarct size after cerebral IR injury by blocking CCR2-mediated inflammation. (A) Quantitative data of infarct size and neurological deficits score 24 h after IR. The data of infarct size represent the mean ± SD (N = 8–12 mice per group), and they were analyzed by one-way ANOVA followed by Bonferroni’s multiple comparison tests. Data of neurological deficits score were analyzed by the nonparametric Kruskal–Wallis test. (B) Quantitative data of cytochrome c in the cytosol fraction 30 min after reperfusion. The data represent the mean ± SD. *P < 0.001 versus saline in the non-ischemic hemisphere, P < 0.001 versus CsA in the noninfarct hemisphere, as analyzed by two-way ANOVA followed by Bonferroni’s multiple comparison tests. I: ischemic hemisphere, N: non-ischemic hemisphere. (C) Quantitative data of infarct size and neurological deficits score 24 h after IR injury. The data of infarct size represent the mean ± SD (N = 6–10), and they were analyzed by one-way ANOVA followed by Bonferroni’s multiple comparison tests. The data of neurological deficits score were analyzed by the nonparametric Kruskal–Wallis test. (D) The effects of Pitava-NP on the infarct size in CCR2-KO mice. The data represent the mean ± SD (N = 10 per group), and they were compared using unpaired t tests.