Abstract: ob＜x＞jective Methods Eighty clean grade healthy male SD rats weighing 280 ~ 350 g and aged 8 ~ 10 weeks were divided into three groups by random number table method: sham operation group (S group, n=20), cardiopulmonary resuscitation group (I/R group, n=30) and hydrogen-rich liquid group (H group, n=30). Cardiopulmonary resuscitation model of cardiac arrest was established by transesophageal electrical stimulation, and only endotracheal intubation and arteriovenous puncture were performed in group S. Immediately after recovery of spontaneous circulation (ROSC) and at 6 hours after ROSC, 5 mL /kg hydrogen-rich solution was intraperitoneally injected, and the other 2 groups were intraperitoneally injected with equal volume normal saline. Neurological function score (NDS) was performed 48 h after ROSC. HE staining was used to observe the cases in CA1 area and count the pyramidal cells. The ex＜x＞pressions of NLRP3, Caspase-1 and ASC in hippocampus were detected by Western blot. Results compared with sham group, the neurological function score and cone cell count of I/R and H groups were decreased after ROSCA48h (P< 0.05). The ex＜x＞pressions of NLRP3, Caspase-1 and ASC in hippocampus were up-regulated (P< 0.05). Compared with I/R group, neurological function score was increased (P< 0.05), pyramid-cell count was increased (P< 0.05), and NLRP3、Caspase-1 and ASC ex＜x＞pressions were down-regulated (P< 0.05). Conclusion The mechanism of hydrogen-rich fluid alleviating brain injury in rats with cardiac arrest/CPR may be related to the inhibition of NLRP3 inflammatory body activation and the alleviation of inflammatory response