Fig. 6

CK2 exerts neuroprotection via promoting mitochondrial fusion in MCAO model. a Scheme of neuroprotection evaluation of ECH in MCAO model. MCAO were established on mice and ECH (50 mg/kg) was administrated for every 2 days, followed by neurological score test in day 9 and bioassay in day 10. b ECH improved neurological score against MCAO insult in CK2α′^+/+ mice, but showed no effect in CK2α′^+/− mice. c ECH protected neurons against MCAO insult in CK2α′^+/+ mice, but showed no effect in CK2α′^+/− mice. Neuroprotection in hippocampal and cortical areas were detected by Nissl staining assay. Arrows indicate Nissl bodies (scale bar: 50 μm). d ECH inhibited cell apoptosis against MCAO insult in CK2α′^+/+ mice, but showed no effect in CK2α′^+/− mice. Cell apoptosis was detected by TUNEL assay (scale bar: 50 µm). e Mfn2 expression was increased by ECH in CK2α′^+/+ mice, but not in CK2α′^+/− mice (scale bar: 50 μm). f ECH-induced mitochondrial fusion was suppressed in CK2α′^+/− mice, which was stained with the specific mitochondrial marker COXIV (scale bar: 50 μm). g CK2α′^+/− blocked ECH-induced Mfn2 expression increase, which was detected by western blot assay. h TCF1/7 significantly translocated into nucleus upon ECH treatment (scale bar: 50 μm). i, j Swimming performance analysis for ECH and IWP-2 neuroprotection in ischemia/reperfusion-induced zebrafishes. Data are expressed as the mean ± SD. ^##P < 0.01 vs. control group. *P < 0.05, **P < 0.01 vs. MCAO group. NS not significant