The present study was designed to investigate the effects of sevoflurane inhalation anesthesia on the cognitive function of rats and to investigate the molecular mechanisms mediating this effect. A total of 100 healthy male Sprague-Dawley rats were divided into four groups: i) Control (air inhalation), ii) low-dose (1.5% sevoflurane inhalation for 2 h), iii) high-dose (3% sevoflurane inhalation for 2 h), and iv) nimodipine group (3% sevoflurane inhalation for 2 h + nimodipine). Sevoflurane inhalation anesthesia resulted in cognitive dysfunction in a dose-dependent manner. Sevoflurane also upregulated the expression of tumour necrosis factor-α (TNF-α), interleukin (IL) -6, -8, and Caspase-3 in the hippocampus. The intervention with nimodipine partially recovered the cognitive function and the abnormal expression of TNF-α, IL-6, IL-8, and Caspase-3 induced by sevoflurane. The results showed that the cognitive dysfunction caused by sevoflurane inhalation in rats may be related to the activation of inflammatory and apoptotic pathways. The neuroprotective effect of nimodipine suggests that abnormal calcium transport is partially responsible for the sevoflurane toxicity.
Keywords: apoptosis protein; cognitive function; interleukin; nimodipine; sevoflurane.