Fig. 2: VK reduced infract volume and promoted sensorimotor and cognitive function in mice subjected to middle cerebral artery occlusion/reperfusion (MCAO/R).

The administration of the VK schedule and behavioral assessment timeline were illustrated schematically (a). Mice (8–10 weeks, males) underwent MCAO for 60 min. The occlusion and reperfusion were confirmed by laser speckle contrast imaging (LSCI). Mice were randomly divided into four groups: sham group, vehicle group, and VK (150 and 300 µg/kg) groups. Mice were administered VK at 0, 4, 22.5, and 46.5 h after MCAO/R as assessed by triphenyl tetrazolium chloride (TTC) staining (b, c) and MRI (d). VK treatment improved sensorimotor recovery as evaluated by the Longa test (e), the rotarod test (f), and the grip test (g) after MCAO/R. The performance in the rotarod test was expressed as the time spent on the rotating rod before falling off and the performance on the grip test was expressed as the score of pullup time for each mouse. Spatial learning and memory were evaluated 11–15 days after MCAO/R by the Morris water maze test. Representative traces indicate the sample paths of the mice from the maze latency trials (learning) (h) and the swimming traces from probe trials (memory) (i). j The latency until the mice located the submerged platform as tested on days 11–14 (defined as spatial learning). k Spatial memory was assessed on day 15 by measuring the time spent swimming in the target quadrant. Statistical analyses were performed by Kruskal–Wallis test with the Dunn post hoc test or two-way repeated-measures ANOVA followed by the Bonferroni post hoc test. Data are expressed as means ± SD, n = 5–7.