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General anesthesia has a great impact on neurodevelopment. However, the mechanisms underlying this effect and therapeutic methods to address it remain limited. The present study aimed to investigate the effects of compound (C)21, a non‑peptide angiotensin II type 2 receptor agonist, on general anesthesia‑induced cerebral injury in neonatal rats. Neonatal Sprague Dawley rats (postnatal day 7) were randomly divided into three groups (n=6 per group): The control, isoflurane and C21+ isoflurane (C21) group. General anesthesia was induced through inhalation of 1.3% isoflurane. Apoptosis and synaptic structure were analyzed. The levels of peroxisome proliferator‑activated receptor (PPAR)‑α were detected using an enzyme‑linked immunosorbent assay. BCL2, apoptosis regulator (Bcl‑2) expression was also measured. Compared with the control group, the cerebral cortex, hippocampus, amygdala and hypothalamus in the isoflurane group had significantly more apoptotic cells (P&lt;0.05). The nuclei of the control group were round and transparent, while shrunken nuclei and condensed chromatin were visible in the isoflurane group. A reduction in synapse number was observed in the isoflurane group compared with the control. By contrast, nuclei shrinkage and the decrease in synaptic number was improved in the C21 group. PPAR‑α and Bcl‑2 expression, at the mRNA and protein levels, was significantly reduced in the isoflurane group compared with the control (P&lt;0.05). C21 treatment reduced the decrease in PPAR‑α and Bcl‑2 in the cerebral cortex, hippocampus, amygdala and hypothalamus (P&lt;0.05). Collectively, it was demonstrated that C21 prevented apoptosis and synaptic loss induced by general anesthesia in neonatal rats by enhancing the expression of PPAR‑α and Bcl‑2.

Effects of compound 21, a non‑peptide angiotensin II type 2 receptor agonist, on general anesthesia‑induced cerebral injury in neonatal rats