Sevoflurane Exacerbates Cognitive Impairment Induced by Aβ_1–40 in Rats through Initiating Neurotoxicity, Neuroinflammation, and Neuronal Apoptosis in Rat Hippocampus

Figure 3

Sevoflurane influenced cognitive function and Aβ_1–42 level in rats. Rats received bilateral intrahippocampus injections of either NS or Aβ_1–40 after training. The spatial probe test was examined in the time course after inhalation of 30% O₂ or 2.5% sevoflurane, and the time spent in exploration of the original platform was recorded (a). The results were expressed as a ratio (%) as compared to the NS + O₂ or Aβ + O₂ group on day 7. Navigation test was performed after inhalation of 30% O₂ or 2.5% sevoflurane on day 7, and the escape latency was recorded (b). The results were expressed as seconds as compared to the NS + O₂ or Aβ + O₂ group at the given times. After the rats inhaled 30% O₂ or 2.5% sevoflurane in the presence and absence of Aβ, hippocampus tissues of the treated rats were harvested. And then, the level of Aβ_1–42 in the supernatant from the tissue was determined by ELISA (c). vs. Aβ + O₂ ().

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(b)

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