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. Author manuscript; available in PMC: 2016 Jun 1.
Published in final edited form as: Stroke. 2015 Apr 28;46(6):1681–1689. doi: 10.1161/STROKEAHA.115.009099

Fig. 6. Impairment of mitochondria function exacerbates stroke outcomes.

Fig. 6

(A) Scheme of experimental design and workflow. Rotenone (1mg/kg, i.p.) or vehicle (saline, i.p.) was administered 30 min prior to right tMCAO (60 min occlusion), BBB permeability was evaluated at 6 hour reperfusion and infarct volume was measured at 24 hour reperfusion. (B) Representative brain coronal sections for Evans blue accumulation and quantitative analysis of Evans Blue extravasation (μg/g brain tissue) in contralateral (left) and ipsilateral (right) hemispheres. Vehicle, n = 4; Rotenone, n = 4. One-way Data are analyzed with ANOVA followed by post-hoc Tukey's test (*, P < 0.05). (C) Representative TTC-stained coronal sections used to analyze infarct of tMCAO mice and quantitative analysis of infarct volumes. Mice treated with rotenone had significant larger infarct volume than vehicle group, in cortex, striatum, and total hemisphere. Rotenone (1 mg/kg, i.p.) or vehicle (saline, i.p.) was administered 30 min prior to right tMCAO (1 hour occlusion) and 24 hour reperfusion was performed. Vehicle, n = 8; Rotenone, n = 8. Data are analyzed with Student's t tests (**, P < 0.01; ***, P <0.001; ****, P < 0.0001.). (D) Rotenone worsened neurological deficits at 6 and 24 hours after tMCAO. Vehicle, n = 12; Rotenone, n = 12. Data are analyzed with Student's t test (****, P < 0.0001).