Effects of sevoflurane general anesthesia during early pregnancy on AIM2 expression in the hippocampus and parietal cortex of Sprague-Dawley offspring rats.

The aim of the present study was to investigate the effect of exposure to sevoflurane general anesthesia during early pregnancy on interferon-inducible protein AIM2 (AIM2) expression in the hippocampus and parietal cortex of the offspring Sprague-Dawley (SD) rats. A total of 18 SD rats at a gestational age of 5-7 days were randomly divided into three groups: i) A control group (control); ii) 2-h sevoflurane general anesthesia, group 1 (S1); and iii) 4-h sevoflurane general anesthesia, group 2 (S2). The six offspring rats in each group were maintained for 30 days and assessed by Morris water maze testing. Brain specimens were collected from offspring rats 30 days after birth. Changes in the structural morphology of neurons in the hippocampus and parietal cortex were observed using hematoxylin and eosin staining. Nissl bodies in the hippocampus and parietal cortex were observed by Nissl staining. The expression of glial fibrillary acidic protein (GFAP), AIM2, CD45 and IL-1β was detected by immunohistochemistry and the protein levels of CD45, IL-1β, pro-caspase-1 and caspase-1 p10 were detected by western blotting. Compared with the control group, offspring rats in the S1 and S2 groups exhibited poor long-term learning and memory ability and experienced different degrees of damage to both the hippocampus and parietal cortex. The expression levels of GFAP, AIM2, CD45, IL-1β, caspase-1 and caspase-1 p10 in the offspring of both the S1 and the S2 groups were significantly increased (P<0.05) compared with offspring of the control group. Moreover, compared with the offspring of the S1 group, hippocampal and parietal cortex injury in the offspring of the S2 group was further aggravated, and the expression of GFAP, AIM2, CD45, IL-1β, pro-caspase-1 and cleaved-caspase-1 was significantly increased (P<0.05). In conclusion, sevoflurane general anesthesia in SD rat early pregnancy promoted the expression of AIM2 and the inflammatory response in the hippocampus and parietal cortex of offspring rats.