Effects of hydrogen-rich fluid on NLRP3 inflammasome expression in the hippocampus of rats with cardiac arrest after cardiopulmonary resuscitation

Objective To evaluate the effects of hydrogen-rich liquid on the expression of NOD-like receptor thermoprotein domain-associated protein 3 (NLRP3) inflammsome in the hippocampus of rats with cerebral injury after cardiac arrest/cardiopulmonary resuscitation (CPR). Methods A total of 80 healthy male SD rats weighing 280-350 g and aged 8-10 weeks were selected. According to the random number table method, they were divided into three groups:a sham operation (Sham) group (n=20), a cardiopulmonary resuscitation (I/R) group (n=30) and a hydrogen-rich liquid (H) group (n=30). A cardiopulmonary resuscitation model of cardiac arrest was established through transesophageal electrical stimulation.Group S was subjected to endotracheal intubation and arteriovenous puncture alone, followed by intraperitoneal injection of 5 ml/kg hydrogen-rich solution immediately after recovery of spontaneous circulation (ROSC) and 6 h after ROSC. The other two groups were intraperitoneally injected with an equal volume of normal saline. Their neurological function score (NDS) was evaluated 48 h after ROSC. The CA1 area and pyramidal cell count were observed by H-E staining. The expression of NLRP3, pro-caspase-1 and apoptosis-associated speck-like protein containinga caspase recruitment domain(ASC) in the hippocampus were detected by Western blot. Results Compared with the Sham group, the I/R and H groups showed decreases in the neurological function score and pyramidal cell count 48 h after ROSC (P<0.05), with up-regulated expression of NLRP3, pro-caspase-1 and ASC in the hippocampus (P<0.05). Compared with the I/R group, the H group presented increases in neurological function score (P<0.05) and pyramidal cells count (P<0.05), as well as down-regulated expression of NLRP3, pro-caspase-1 and ASC(P<0.05). Conclusions Hydrogen-rich fluid can alleviate brain injury in rats with cardiac arrest/cardiopulmonary resuscitation, which may be related to inhibiting the activation of NLRP3 inflammsomeand alleviating inflammatory response.