Abstract

To investigate the effect and related mechanism of propofol anesthesia on pyroptosis in neonatal rat hippocampus. Neonatal rats were divided into a control group (injected intraperitoneally with saline), a propofol group (injected intraperitoneally with 80 mg/kg propofol) and a propofol+MCC950 group (injected intraperitoneally with 80 mg/kg propofol and 10 mg/kg MCC950) and administered for 5 d. The day after the end of drug administration, hippocampi were analyzed for pyroptosis by transferase dUTP nick end labeling assay and for interleukin beta-1, interleukin-18 levels, nod-like receptor protein 3, ASC and caspase-1 protein expression in the hippocampus were determined by Western blotting; at the end of drug administration on the 19th d, the escape latency, the number of crossing the platform and the percentage of time spent in the target quadrant were recorded in the water maze test. Pyroptosis, levels of interleukin-beta and interleukin-18 and the protein levels of nod-like receptor protein 3, ASC and caspase-1, as well as the escape latency of the rats of hippocampal tissues were significantly higher in the propofol group than those in the control group (p<0.05) and the percentage of time crossing the platform and staying in the target quadrant was significantly lower (p<0.05) in the propofol group than those in the control group; pyroptosis, levels of interleukin-beta and interleukin-18 and the protein levels of nod-like receptor protein 3, ASC and caspase-1, as well as the escape latency of the rats of propofol+MCC950 group were significantly lower in the propofol group than those in the control group (p<0.05), whereas the number of crossing the platform and the percentage of time spent in the target quadrant were significantly higher (p<0.05). Propofol anesthesia may trigger inflammatory responses by activating the nod-like receptor protein 3/caspase-1 pathway, which in turn induces pyroptosis in the neonatal rat hippocampus, leading to reduced learning and memory performance.