Esketamine reduced acute lung injury caused by limb ischemia-reperfusion in a rat model. Treatment lowered pulmonary edema, inflammatory cell infiltration, and oxidative stress, as shown by decreased MDA and increased SOD levels. It also reduced inflammatory cytokines in bronchoalveolar fluid and serum. The protective effect involved suppression of the TLR4/NF-κB/NLRP3 pathway; activating that pathway with LPS reversed esketamine's benefits. The findings suggest esketamine may be a potential therapy for acute lung injury.
In a mouse model of depression induced by chronic social defeat stress, susceptible mice showed reduced social interaction, lower sucrose preference, decreased NRG1 protein expression in the prefrontal cortex, and increased immobility time compared to controls. A subanesthetic dose of esketamine increased NRG1 expression in the prefrontal cortex within 30 minutes and improved social interaction and reduced immobility at both 30 minutes and 24 hours post-injection. No significant changes were observed in GAD67 or ErbB4 expression. Esketamine may rapidly improve depressive-like behavior by regulating the NRG1-ErbB4 signaling pathway.