Active abdominal compression‑decompression cardiopulmonary resuscitation attenuates neuroinflammation associated with TLR4/NF‑κB signaling in a rat model of cardiac arrest

Cardiac arrest (CA) induces cerebral ischemia‑reperfusion injury, which is a major contributor to mortality and neurological dysfunction following resuscitation. Active abdominal compression‑decompression cardiopulmonary resuscitation (AACD‑CPR) has emerged as a potential alternative to standard cardiopulmonary resuscitation (STD‑CPR). The present study aimed to investigate whether AACD‑CPR attenuates neuroinflammation after CA/CPR and whether this effect is associated with changes in Toll‑like receptor 4/nuclear factor‑κB (TLR4/NF‑κB)‑related signaling. A rat model of CA was established, followed by resuscitation with either STD‑CPR or AACD‑CPR. Return of spontaneous circulation (ROSC), survival, NDS and neuronal injury were evaluated. The expression levels of TLR4, NF‑κB and inflammation‑related markers, including tumor necrosis factor‑α, interleukin‑1 β, glial fibrillary acidic protein (GFAP) and ionized calcium‑binding adapter molecule 1 in brain tissue were assessed by western blotting and immunohistochemistry. Compared with STD‑CPR, AACD‑CPR markedly reduced resuscitation duration and improved early neurological outcomes. Although the ROSC rate and short‑term survival rate were numerically higher in the AACD‑CPR group than in the STD‑CPR group, these differences did not reach statistical significance and therefore should not be interpreted as evidence of a definitive survival benefit. AACD‑CPR was also associated with reduced neuronal injury, decreased expression of proinflammatory cytokines and glial activation markers and downregulation of TLR4/NF‑κB‑related proteins in brain tissue. AACD‑CPR improved early neurological outcomes and attenuated neuroinflammatory responses in this rat model of CA/CPR. These effects were accompanied by suppression of TLR4/NF‑κB‑related signaling. However, as this was a preclinical small‑animal study, the findings should be interpreted cautiously and not as evidence that AACD‑CPR can clinically replace STD‑CPR. Further studies in large‑animal models and well‑designed clinical investigations are required to validate its safety, feasibility and translational relevance.