Sevoflurane aggregates cognitive dysfunction and hippocampal oxidative stress induced by β-amyloid in rats

AimsTo investigate the effects of sevoflurane inhalation on β-amyloid (Aβ)-induced cognitive disorders and hippocampal oxidative stress in rat models.Materials and methodsCognitive dysfunction is induced by hippocampal injection of Aβ1–40 (10 μg in 2 μl) for 22 days. To explore the effect of sevoflurane inhalation on Aβ1–40 induced cognitive disorder, two doses of sevoflurane inhalation are used: 1.3% (Aβ + S1) and 2.6% (Aβ + S2). Sham operation (Sham, for operation control), saline injection (Control, for injection control) and 30% oxygen inhalation after Aβ1–40 injection (Aβ + O2, for inhalation control) were used as controls. All rats were further tested in electrical Y-maze and Morris water maze. Serum S100β levels, hippocampal superoxide dismutase (SOD) activity, S100β expression and malonyldialdehyde (MDA) concentrations were further quantified.Key findingsRats in Aβ + O2, Aβ + S1 and Aβ + S2 groups had lower number of correct actions in the electrical Y maze task, longer escape latencies, less time exploring the original platform, elevated serum S100β levels, depressed hippocampal SOD activity, S100β expression and higher MDA concentrations compared to control group (p < 0.05). Such difference was not significant between Aβ + S1 and Aβ + O2 rats. Rats in Aβ + S2 group, however, showed significantly impaired performances compared to those in Aβ + S1 group (p < 0.05).SignificanceSevoflurane (2.6%) can aggravate the Aβ-induced cognitive dysfunction, possibly via the intracerebral oxidative stress response.