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

Abstract

To investigate the effects of sevoflurane inhalation on β-amyloid (Aβ)-induced cognitive disorders and hippocampal oxidative stress in rat models. Cognitive dysfunction is induced by hippocampal injection of Aβ1-40 (10μg in 2μl) for 22days. 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. Rats 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). Sevoflurane (2.6%) can aggravate the Aβ-induced cognitive dysfunction, possibly via the intracerebral oxidative stress response.