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. 2020 Feb 7;45(4):1176–1186. doi: 10.3892/ijmm.2020.4493

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Copyright: © Fu et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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CORM-3 inhibits the interaction between NLRP3 and ASC in the hippocampus after HSR. (A) Co-immunoprecipitation assay with an anti-ASC antibody; hippocampal tissue was immunoblotted with anti-NLRP3, anti-pro-caspase-1 and anti-ASC antibodies. (B and C) Optical density values of (B) NLRP3 and (C) pro-caspase-1 in the hippocampal tissue evaluated by western blotting. Data are presented as the mean ± SD (n=6 per group). ^*P<0.05 vs. Sham; ^#P<0.05 vs. HSR iCORM-3. CORM, carbon monoxide-releasing molecule; HSR, hemorrhage shock and resuscitation; iCORM-3, inactive CORM-3; NLRP3, nucleotide-binding oligomerization domain-like receptors pyrin domain-3; ASC, apoptosis-associated speck-like protein containing a CARD domain.