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. 2019 Jun 20;10(7):487. doi: 10.1038/s41419-019-1716-9

Fig. 1. Necroptosis activated after ischemic stroke in Endothelium.

Fig. 1

a, b Representative images and statistical results of PI (red, represents necrosis)/TUNEL (green, represents apoptosis) staining of cerebral cortex at 6 h, 12 h, 1 day, 3 day, and 7 day after tMCAO. n = 5; *P < 0.01 vs. Sham group, **P < 0.0001 vs. Sham group; Scale bar: 100 μm. c, d Representative images and statistical results of CD31 (green) and PI (red) staining of rat brain sections from Sham and tMCAO (12 h, 1 day, 3 day, 7 day) groups. Arrows indicate the colocalization of CD31 and PI. n = 6; *P < 0.01 vs. Sham group, **P < 0.0001 vs. Sham group. Scale bar: 50 μm. e–i Expression levels of p-RIP1/RIP1, p-MLKL/MLKL, Casp 3 and Casp 8 in lateral cortex tissues of the peri-infarct area after tMCAO (3 day). n = 6; *P < 0.05 vs. Sham group; **P < 0.01 vs. Sham group. j Representative electron microscopy images of EC from ischemic cortex after tMCAO (3 day). EC from ischemic cortex exhibited translucent cytoplasm, swelling mitochondria, and membrane breakdown. n = 3; Scale bar: 2 μm (merged pictures) and 1 μm (magnified pictures). k, i Representative images and statistical results of CD31 (green) and p-MLKL (red) staining of rat brain sections from Sham and tMCAO (3 day) groups. Arrows indicate the colocalization of CD31 and p-MLKL. Scale bar: 100 μm (merged pictures) and 50 μm (magnified pictures); n = 6; tMCAO group 26.50 ± 1.176% vs. Sham group 1.833 ± 0.3073%; **P < 0.001 (All values from three to six independent experiments are presented as mean ± S.E.M.)