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. 2020 Jul 23;11(7):565. doi: 10.1038/s41419-020-02770-w

Fig. 5. RIP3 deficiency protects against cerebral damage after MCAO/R by attenuating necroptosis and neuroinflammation.

Fig. 5

a Representative TTC-stained images of brain slices in WT mice and Rip3−/− mice at 24 h after MCAO/R. b Comparison of the percentages of infarct volume between WT mice and Rip3−/− mice. Each symbol represents one male mouse (n = 10). Bars indicate the means ± SEM; P-values were determined using a t-test: *P < 0.05. c–e Comparison of neurological scores between WT mice and Rip3−/− mice at 24 h after MCAO/R (n = 20): Longa score (c), Clark general score (d), and Clark focal score (e). Data in bar graphs are means ± SEM; t-test: ns not significant; **P < 0.01. f TUNEL staining of the infarct area of WT and Rip3−/− mice after MCAO/R. Scale bar, 50 μm. g Cytokine and chemokine expressions in the infarct area from WT mice and Rip3−/− mice in the sham group and the MCAO/R group were detected by RT-PCR (n = 6). Data in bar graphs are means ± SEM; t-test: ns not significant; *P < 0.05, **P < 0.01. h Brain samples of the infarct area from WT mice and Rip3−/− mice were analyzed by immunoblotting to examine activation of the NK-κB pathway and MAPK pathway (n = 6).