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Fig. 4 | Journal of Neuroinflammation

Fig. 4

From: Endogenous hydrogen sulphide attenuates NLRP3 inflammasome-mediated neuroinflammation by suppressing the P2X7 receptor after intracerebral haemorrhage in rats

Fig. 4

The effects of SAM and NaHS administration on NLRP3 inflammasome activation and IL-1β maturation. a Quantitative analysis of NLRP3 mRNA levels by qPCR in the sham, vehicle, SAM and NaHS groups at 1 day after ICH. NLRP3 mRNA levels were apparently increased in the vehicle group at 1 day after ICH (p < 0.01 vs. sham). SAM and NaHS treatment significantly reduced NLRP3 mRNA expression in their respective treatment groups compared to the vehicle group (p < 0.05). The relative densities of each mRNA have been normalized against those of the vehicle group. bf Representative bands and quantitative analysis of NLRP3, ASC, caspase-1 p20 subunit and mature IL-1β levels in the perihaematomal tissues of the sham, vehicle, SAM and NaHS groups at 1 day after ICH. The protein levels of the NLRP3 inflammasome components, including the protein levels of NLRP3, ASC and caspase-1, and the levels of IL-1β production were evidently elevated in the vehicle group at 1 day after ICH (p < 0.01 vs. sham). SAM and NaHS treatment significantly suppressed NLRP3 inflammasome component expression and the subsequent secretion of mature IL-1β (p < 0.05 vs. vehicle). The relative densities of each protein have been normalized against those of the vehicle group. N = 6 rats per group. Data are presented as the mean ± SEM. **p < 0.01 vs. sham; #p < 0.05 vs. vehicle. SAM S-adenosyl-l-methionine, GAPDH glyceraldehyde 3-phosphate dehydrogenase, ICH intracerebral haemorrhage, IL interleukin, NLRP3 pyrin domain-containing 3, ASC adaptor protein apoptosis-associated speck-like protein containing a CARD

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