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

Figure 5

Sevoflurane inhalation influenced protein expression of Bcl-xL, caspase-9, BDNF, RAGE, and mRNA level of IL-1β, NF-κB, and iNOS in the hippocampus. Caspase-9 (a, b), Bcl-xL (a, c), BDNF (d, e), and RAGE (d, f) protein levels in the NS- or Aβ-treated hippocampus of rats were determined using Western blot after inhaling 30% O₂ and 2.5% sevoflurane at the indicated times. Relative band intensity of each protein expression was calculated as % of the intensity of the β-actin protein band and expressed as a fold change in reference to their controls. IL-1β (g), NF-κB (h), and iNOS (i) mRNA levels in the NS- and Aβ-treated hippocampus were determined after inhaling 30% O₂ or 2.5% sevoflurane on day 7. The results were expressed as a fold change in reference to mRNA levels of their own controls. vs. A β + O₂ (); vs. A β + O₂ ().

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