This study demonstrates that recombinant human thymosin β4 (rhTβ4) significantly improves survival and reduces organ damage in endotoxemia models by suppressing inflammatory cytokine cascades, macrophage activation, and oxidative stress via TLR4/NF-κB inhibition. The research also shows rhTβ4 rescues cognitive deficits and neuronal damage by suppressing microglial overactivation through LPAR3 downregulation. These findings position thymosin β4 as a multi-organ protective agent against sepsis-related complications including acute lung injury and encephalopathy—conditions with high mortality and no targeted treatments. The mechanistic clarity and robust efficacy make this highly relevant for practitioners seeking evidence-based interventions in critical care and inflammatory disease management.
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rhTβ4 reduced lung injury and cognitive deficits in sepsis models via TLR4/NF-κB and microglial suppression—multi-organ protection worth monitoring in critical care research.