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. 2020 Apr 30;9(9):e014920. doi: 10.1161/JAHA.119.014920

Figure 6. CARD3 induced ischemia‐reperfusion (I‐R) injury via activating TAK1.

Figure 6

A, TAK1 (transforming growth factor‐β‐activated kinase 1) specific inhibitors, 5Z‐7‐oxozeaenol (5Z‐7‐O) were intravenously administrated into non‐transgenic (NTG) or neuron‐specific CARD3‐TG mice 30 minutes before suffering cerebral ischemia, and dimethyl sulfoxide (DMSO) was injected as control. After reperfusion for 24 hours, brain sections of the indicated group were stained with TTC (2,3,5‐triphenyltetrazolium chloride) (left) and quantitative analysis of infarct volume (right) was performed. Data were exhibited as mean±SD. Statistical analysis was performed by Student t test, *P<0.05 vs their control group, n=6 mice per group. B through D, brain homogenates of the indicated group were obtained after reperfusion for 6 hours. And the level of the indicated proteins were analyzed with Western blotting, n=4 mice per group. Data were exhibited as mean±SD. Statistical analysis was performed by one‐way analysis of variance (ANOVA), followed by Bonferroni post hoc or Tamhane's T2 analysis, *P<0.01, **P<0.01, ***P<0.001 vs the NTG group treated with DMSO or 5Z‐7O, and ##P<0.01, ###P<0.001 vs the CARD3‐TG group treated with DMSO. GAPDH served as a loading control, n=4 mice per group. JNK indicates c‐Jun N‐terminal kinase; p38, p38 mitogen‐activated protein kinase; Bcl2 indicates B‐cell lymphoma‐2; IKKβ, inhibitor of nuclear factor kappaB kinase beta; IKBα, inhibitor of nuclear factor kappa‐B α; and p65, nuclear factor kappa‐B RelA(p65).