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In lipopolysaccharide (LPS)-induced endotoxemia in mice, a model where LPS potently stimulates inflammation, the ALA treatment suppressed NF-κB activation, reduced the levels of proinflammatory cytokines (TNF-α, MCP-1) and adhesion molecules (VCAM-1, ICAM-1, E-selectin) in the lungs and heart, and activated the PI3K/Akt pathway