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. 2021 Mar 4;22(5):2549. doi: 10.3390/ijms22052549

Figure 1.

Figure 1

A possible mechanism of H2 on inflammatory diseases targeting the mtROS production and NLRP3 inflammasome activation. H2 can selectively eliminate ·OH generated inside of mitochondria, and inhibit the cascade leading to NLRP3 activation by scavenging excess mtROS, and this inhibition leads to the suppression of IL-1β and IL-18 production. ROS: reactive oxygen species; ·OH: hydroxyl radicals; H2: molecular hydrogen; IL-1β: interleukin-1β; IL-18: interleukin-18; NLRP3: nucleotide-binding and oligomerization domain-like receptor family pyrin domain-containing 3; TLR4: toll-like receptor 4; PAMPs: pathogen-associated molecular patters; DAMPs: damage-associated molecular patters; ASC: apoptosis-associated speck-like protein containing a CARD; LPS: lipopolysaccharide; mtROS: mitochondrial reactive oxygen species; mtDNA: mitochondrial DNA; CMPK2: cytidine/uridine monophosphate kinase 2.