Abstract
This study aimed to observe the recent spatial recall ability and the changes of expression of hippocampal apolipoprotein E (ApoE) and amyloid β protein (Aβ) in adult rats after inhaling sevoflurane anesthetic drugs, and to analyze the mechanism of action. For this purpose, a total of 54 adult SD clean-grade rats were selected in this study and were randomly divided into the sevoflurane anesthesia group, carrier gas group and control group, 18 rats in each group. The rats in the carrier gas group were inhaled with 1 L/min of oxygen O2+1 L/min air mixed carrier gas for 2 h, and the rats in the sevoflurane anesthesia group were given 3.2%sevoflurane for 2 hours based on the carrier gas group, the control rats were naturally reared. Before the model was copied, the Morris water maze experiment was performed before the material was taken. Some rat brain tissues were extracted on the first day (T1), the third day (T3), and the seventh day (T7) after model replication. The immunohistochemistry was used to measure the mean optical density (MOD) value of APOE and Aβ in hippocampal CA1, CA3 and DG regions. The indicators above at different time points of each group were compared and analyzed. Results showed that the number of crossing the original platform at each time point, the residence time of the original platform quadrant, the number of entering the original platform quadrant, and the percentage of the original platform quadrant residence time in the sevoflurane anesthesia group and the carrier gas group were compared, and there were no significant differences between two groups (P>0.05). Compared with the carrier gas group, the MOD values of APOE in the hippocampus at T1 and T3 time points in the sevoflurane anesthesia group were decreased (P<0.05), the MOD values of Aβ in the hippocampus at the T7 time point were increased (P<0.05). It concluded that Inhalation of 3.2%sevoflurane has no obvious damage to the recent spatial recall ability of adult rats. Within 7 days after inhalation of 3.2% sevoflurane, it can inhibit hippocampus Aβ deposition through down-regulating APOE expression level. The critical time point for hippocampal Aβ increasing was 7 days after anesthesia.
Highlights
In recent years, the incidence of postoperative cognitive dysfunction (POCD) in patients has increased year by year, and the situation is extremely severe
Results showed that the number of crossing the original platform at each time point, the residence time of the original platform quadrant, the number of entering the original platform quadrant, and the percentage of the original platform quadrant residence time in the sevoflurane anesthesia group and the carrier gas group were compared, and there were no significant differences between two groups (P>0.05)
The brain tissues of rats were extracted on day 1 (T1), day 3 (T3) and day 7 (T7) after model replication, and the mean optical density (MOD) of APOE and amyloid β protein (Aβ) in hippocampal CA1, CA3 and DG regions were detected by immunohistochemistry
Summary
The incidence of postoperative cognitive dysfunction (POCD) in patients has increased year by year, and the situation is extremely severe. Β and γ-secretase produce Aβ by continuous action on amyloid precursor protein (APP). Related literature has confirmed that inhalation of anesthetic drugs, such as sevoflurane, has a serious impact on the aggravation of hippocampal Aβ deposition, which in turn impairs the learning and memory ability of rats. In this process, various factors are involved and have different degrees of influence, among which, the effect of apolipoprotein E (ApoE) gene polymorphism on APP is mainly showed as the abnormal degradation of APP, leading a large amount of Aβ deposition, which seriously damages the biofilm and the stability of intracellular calcium ions
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