{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,20]],"date-time":"2026-03-20T08:38:23Z","timestamp":1773995903063,"version":"3.50.1"},"reference-count":54,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,3,20]],"date-time":"2026-03-20T00:00:00Z","timestamp":1773964800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>\n                      The liver is extremely vulnerable to endotoxin-induced damage during sepsis. Hydrogen gas (H\n                      <jats:sub>2<\/jats:sub>\n                      ) is a colorless and odorless gas molecule with anti-oxidative and anti-inflammatory actions. However, the effects of H\n                      <jats:sub>2<\/jats:sub>\n                      intraperitoneal injection on sepsis-induced acute liver injury and the possible mechanisms remain unclear.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      Biochemical analysis, H&amp;amp;E staining, immunoblotting, immunofluorescence, and TUNEL staining were used to investigate the effects and mechanisms of H\n                      <jats:sub>2<\/jats:sub>\n                      intraperitoneal injection on lipopolysaccharide (LPS)-induced acute liver injury in mice. AML12 cells and pharmacological rescue experiment were used to confirmed the target of H\n                      <jats:sub>2<\/jats:sub>\n                      .\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      H\n                      <jats:sub>2<\/jats:sub>\n                      pretreatment by intraperitoneal injection improved LPS-induced acute liver injury in mice as indicated by reducing inflammatory cells infiltration in the liver, down-regulating serum ALT and AST levels, decreasing hepatic 3-nitrotyrosine, MDA, and MPO levels, and up-regulating hepatic GSH levels. Mechanistically, H\n                      <jats:sub>2<\/jats:sub>\n                      suppressed TLR4 to IKK-NF-\u03baB and to MAPK (ERK, p38 and JNK) signaling, and thus reducing pro-inflammatory cytokines, including TNF-\u03b1, IL-1\u03b2, and IL-18 levels in the liver of LPS-challenged mice. Moreover, the hepatic pyroptosis signaling including NLRP3 inflammasome (NLRP3, ASC, and Caspase-1) to GSDMD, Caspase-8\/11 to GSDMD, Caspase-3 to GSDME, and TUNEL staining in LPS-challenged mice were all reversed by H\n                      <jats:sub>2<\/jats:sub>\n                      treatment. The pharmacological rescue experiments by agonist (nigericin) and antagonist (MCC950) of NLRP3 further confirm the action of H\n                      <jats:sub>2<\/jats:sub>\n                      on NLRP3\n                      <jats:italic>in vitro<\/jats:italic>\n                      .\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>\n                      H\n                      <jats:sub>2<\/jats:sub>\n                      pretreatment by intraperitoneal injection alleviated LPS-induced acute liver injury in mice by modulating redox homeostasis, TLR4-mediated innate immune signaling, NLRP3 inflammasome activation and pyroptosis signaling.\n                    <\/jats:p>\n                  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