Figure 6.

Adiponectin contributes to RF-induced neuroprotection against tFCI. (a) Representative immunofluorescent images of MAP2 staining seven days after tFCI in wild-type (WT) and adiponectin knockout (Adipo^−/−) mice. Dashed line depicts infarct region. (b) Measurement of infarct volume in WT and Adipo^−/− mice indicates that knockout of adiponectin exacerbates ischemic injury in RF-fed mice. No significant difference was detected between WT and Adipo^−/− in LF-fed mice. n = 10/group, *p ≤ 0.05 between groups as indicated. (c–e) Sensorimotor deficits induced by tFCI were significantly alleviated in both wild type and Adipo^−/− mice pretreated with RF within seven days after ischemic insult. RF-induced improvements in sensorimotor function as assessed in the rotarod (c) and grid walking test (d, e) were partly abolished by knockout of adiponectin. *p ≤ 0.05, **p ≤ 0.01 between groups as indicated. Brackets indicate comparisons within genotypes between LF and RF treatment (red, WT; blue, Adipo^−/−). *p ≤ 0.05, **p ≤ 0.01, ***p ≤ 0.001 Adipo^−/− RF vs. Adipo^−/− LF; ^###p ≤ 0.001 WT RF vs. WT LF. Data are mean ± SD. n = 10 mice per group.