Fig. 7

MCC950 treatment improves survival, neurologic outcome, neurocognitive function, and neuropathological damage after cardiac arrest. a Kaplan–Meier analyses of cumulative survival during 7-day follow-up after ROSC. Solid line, vehicle group (n = 22); dashed line, MCC950 group (n = 22). b Neurologic deficit scores (NDS; 0 = brain death; 80 = normal) of survived rats at 24, 48, 72 h, and on day 7 after ROSC. c Scatter plots reflecting the difference in distribution of NDSs between the vehicle and MCC950 groups. d–f The effect of MCC950 on post-cardiac arrest spatial memory and learning deficits assessed by Morris water maze analysis, including the mean latency in searching the hiding platform (d), the frequency of crossing the platform area, and percentage of time spent in the target quadrant (Q3) during the probe trial (e, f). g, h The effect of MCC950 on post-cardiac arrest neuropathological damage characterized by the changes in Nissl staining and immunohistochemical staining for NeuN, GFAP, MAP-2, Iba-1, and CD68. Scale bar = 500 μm or 100 μm. The data in panels a, b, and c are analyzed using non-parametric test, and the other data are analyzed via parametric test. Data are presented as mean ± SD or medians and 25th to 75th percentiles (NDSs). Statistical significances are determined with one-way ANOVA followed by Tukey’s post hoc test or by Mann–Whitney U test (NDSs). *P < 0.05, **P < 0.01, ***P < 0.001 versus sham (n = 5); #P < 0.05, ##P < 0.01, ###P < 0.001 versus vehicle