RESUMEN
Objective To evaluate the effect of α7 nicotinic acetylcholine receptor (α7nAChR) agonist on inflammasome of NOD-like receptor pyrin domain containing 3 ( NLRP3) during brain injury in-duced by cardiopulmonary bypass ( CPB) in rats. Methods Twenty-four clean-grade adult male Sprague-Dawley rats, weighing 350-450 g, were randomly divided into sham operation group (group S), group CPB, and CPB plusα7nAChR agonist PHA568487 group (group CP) after 5-day Morris water maze train-ing, with 8 rats in each group. Group S was mechanically ventilated for 60 min without receiving CPB. Group CPB received CPB for 60 min. PHA 5684870. 8 mg/kg was intraperitoneally injected at 30 min be-fore CPB in group CP. Water maze test was performed on 3rd day after operation to record the escape laten-cy and times of crossing the original platform. The rats were sacrificed at 2 h after the behavioral test, and their hippocampi were harvested for determination of cell apoptosis ( by TUNEL) and contents of interleukin-1beta ( IL-1β) and IL-18 ( by enzyme-linked immunosorbent assay) , caspase-1 activity ( by using spectro-photometry) , expression of NLRP3, apoptosis-associated speck-like protein containing a CAR ( ASC) and pro-caspase-1 ( by Western blot or real-time polymerase chain reaction) , and expression of NLRP3, ASC and caspase-1 mRNA (using real-time polymerase chain reaction). Apoptotic index (AI) was calculated. Results Compared with group S, the escape latency was significantly prolonged, the times of crossing the original platform were decreased, the AI, contents of IL-1β and IL-18 and caspase-1 activity were in-creased, and the expression of NLRP3 and ASC protein and mRNA, pro-caspase-1 and caspase-1 mRNA was up-regulated in CPB and CP groups (P＜0. 05). Compared with group CPB, the escape latency was significantly shortened, the times of crossing the original platform were increased, the AI, contents of IL-1β and IL-18 and caspase-1 activity were decreased, and the expression of NLRP3 and ASC protein and mRNA, pro-caspase-1 and caspase-1 mRNA was down-regulated in group CP (P＜0. 05). Conclusion The mechanism by whichα7nAChR agonist alleviates CPB-induced brain injury may be related to inhibiting NLRP3 inflammasome and reducing inflammatory responses in brain tissues of rats.