Sevoflurane Exacerbates Cognitive Impairment Induced by A[[beta].sub.1-40] in Rats through Initiating Neurotoxicity, Neuroinflammation, and Neuronal Apoptosis in Rat Hippocampus

• Published in: Mediators of inflammation 2018-01, Vol.2018
• Main Authors: Tian, Yue, Chen, Ke-yan, Liu, Li-dan, Dong, Yun-xia, Zhao, Ping, Guo, Shan-bin
• Format: Article
• Language: English
• Subjects: Anesthetics; Apoptosis; Brain; Neurons; Nitric oxide; Sevoflurane
• ISSN: 0962-9351
• DOI: 10.1155/2018/3802324

Objective. This study was aimed at investigating whether sevoflurane inhalation induced cognitive impairment in rats with a possible mechanism involved in the event. Methods. Thirty-two rats were randomly divided into four groups of normal saline (NS) + [O.sub.2], NS + sevoflurane (sevo), amyloid-[beta] peptide (A[beta]) + [O.sub.2], and A[beta] + sevo. The rats in the four groups received bilateral intrahippocampus injections of NS or A[beta]. The treated hippocampus was harvested after inhaling 30% [O.sub.2] or 2.5% sevoflurane. Evaluation of cognitive function was performed by Morris water maze (MWZ) and an A[[beta].sub.1-42] level was determined by ELISA. Protein and mRNA expressions were executed by immunohistochemical (IHC) staining, Western blotting, and qRT-PCR. Results. Compared with the NS-treated group, sevoflurane only caused cognitive impairment and increased the level of A[[beta].sub.1-42] of the brain in the A[beta]-treated group. Sevoflurane inhalation but not [O.sub.2] significantly increased glial fibrillary acidic protein (GFAP) and ionized calcium-binding adaptor molecule (IBA)1 expression in A[beta]-treated hippocampus of rats. Expression levels for Bcl-xL, caspase-9, receptor for advanced glycation end products (RAGE) and brain-derived neurotrophic factor (BDNF) were significantly different in quantification of band intensity between the rats that inhaled [O.sub.2] and sevoflurane in Aft-treated groups (all P