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Fig. 4 | Journal of Neuroinflammation

Fig. 4

From: NLRP3 inflammasome-mediated microglial pyroptosis is critically involved in the development of post-cardiac arrest brain injury

Fig. 4

Cardiac arrest induces the activation of NLRP3 inflammasome in microglia. a Confocal analysis of NLRP3 (orange) and several cell markers (green) including Iba-1, GFAP, NeuN, CD31, NG2, and Olig2 staining and merged images 12 h after ROSC. b Confocal microscopy of caspase-1 (red) and several cell markers (green) including Iba-1, GFAP, NeuN, CD31, NG2, and Olig2 staining and merged images 12 h after ROSC. c The quantitative analysis of the distribution of NLRP3- or caspase-1-positive cells in above types of cells, which represents 50 cells per rat and 5 rats per group. d Confocal analysis of NLRP3 (orange) and caspase-1 (red) staining and merged images 12 h after ROSC. Scale bar = 50 μm or 25 μm. eh The association of NLRP3, ASC, and caspase-1 detected by immunoprecipitation, in both cortex and hippocampus 12 h after cardiac arrest. The quantification of hippocampus (f) and cortex (h) is normalized to the level of corresponding inflammasome components from sham group. Samples from post-cardiac arrest rats are immunoprecipitated with isotype IgG as a control. All data in this figure are analyzed using parametric test. Data are represented as mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001 versus sham group. n = 5–6 per group. CA/CPR cardiac arrest and cardiopulmonary resuscitation

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