Skip to main content
. 2024 Sep 20;15:1444740. doi: 10.3389/fimmu.2024.1444740

Table 3.

Protective mechanisms of SPMs against septic liver injury.

SPMs Model concentration/dose and application Mechanisms of intervention Effect/outcome Reference
LXA4 LPS intraperitoneal injection LXA4 10μg/kg injected intraperitoneally TLR4 signaling pathway IL-6 and TNF-α↓, expression of TLR4 and TRAF6↓ (45)
RVD1 LPS/d-GalN mouse model RvD1 (0.1 or 1 μg) injected intraperitoneally Inflammatory cells/cytokines Neutrophil population↓, HMGB1, TNF-α, IL-6, IL-10 and MCP-1↓ (44)
Apoptosis Tunel hepatocytes↓
MaR1 CLP 1 ng of MaR1 injected via the tail vein (34)
100 ng/mouse of MaR1 intraperitoneally (48)
Inflammatory response NF-κB activation↓, IL-1β, TNF-α and IL-6↓ (34) (48)
LPS/D-GalN mouse model MaR1 (100ng, i.v.) Lipid Peroxidation GSH and GSH/GSSG↑, ROS↓ (47)
Ferroptosis Nrf2, HO-1 and GPX4↑, ferroptosis-induced liver injury↓
MaR1 (50 and 100 ng) by tail vein injection Inflammatory response MAPK/NF-κB activation↓, IL-1β, TNF-α and IL-6↓ (46)
Pyroptosis NLRP3 and p30-GSDMD↓

D-galactosamine (D-GalN); TNF receptor associated factor 6 (TRAF6); high mobility group protein B1 (HMGB1); macrophage chemotactic protein (MCP)-1; glutathione/oxidized glutathione (GSH/GSSG); NLR family pyrin domain-containing 3 (NLRP3); Gasdermin D (GSDMD); mitogen-Activated Protein Kinase (MAPK); nuclear Factor-κB (NF-κB); ↑ represents an increase in level; ↓ represents a decrease in level.