Sevoflurane Induces Hippocampal Neuronal Apoptosis by Altering the Level of Neuropeptide Y in Neonatal Rats

Kang, Wenbin; Lu, Danbo; Yang, Xiaoyu; Ma, Wudi; Chen, Xi; Chen, Keyu; Xu, Xuanxian; Zhou, Xue; Zhou, Lihua; Feng, Xia

doi:10.1007/s11064-020-03028-9

Cited by 12 publications

(9 citation statements)

References 41 publications

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“…[25][26][27]29,30,54,61,62 Finally, we specifically examined peptide changes on a very short time-scale (<5 min total). This contrasts with many prior studies, which examine extended periods of anesthetic administration [24][25][26][29][30][31]65 or measure the changes at time points long after administration (≥30 min). 54,61,64 Our study thus provides valuable insight into any rapid changes in pituitary peptides that may occur in a typical peptidomics study.…”

Section: ■ Results and Discussionmentioning

confidence: 88%

“…Anesthetic use during a peptidomics experiment may alter the concentration or the enzymatic processing of peptides being measured, which may obscure changes resulting from experimental variables that are of real interest to researchers. Indeed, some prior studies suggest that common anesthetics like isoflurane, halothane, sevoflurane, or nitrous oxide can influence the levels of targeted cell–cell signaling peptides in the CNS, over either long-term or acute exposure. − However, how anesthetics change the measured peptide abundances over the course of a typical peptidomics experiment, or what proportion of peptides may be affected, are unanswered questions.…”

Section: Introductionmentioning

confidence: 99%

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Short-Term Administration of Common Anesthetics Does Not Dramatically Change the Endogenous Peptide Profile in the Rat Pituitary

Mousavi

Qiu

Heinis

et al. 2022

ACS Chem. Neurosci.

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Cell−cell signaling peptides (e.g., peptide hormones, neuropeptides) are among the largest class of cellular transmitters and regulate a variety of physiological processes. To identify and quantify the relative abundances of cell−cell signaling peptides in different physiological states, liquid chromatography−mass spectrometry-based peptidomics workflows are commonly utilized on freshly dissected tissues. In such animal experiments, the administration of general anesthetics is an important step for many research projects. However, acute anesthetic administration may rapidly change the measured abundance of transmitter molecules and metabolites, especially in the brain and endocrine system, which would confound experimental results. The aim of this study was to evaluate the effect of short-term (<5 min) anesthetic administration on the measured abundance of cell−cell signaling peptides, as evaluated by a typical peptidomics workflow. To accomplish this goal, we compared endogenous peptide abundances in the rat pituitary following administration of 5% isoflurane, 200 mg/kg sodium pentobarbital, or no anesthetic administration. Label-free peptidomics analysis demonstrated that acute use of isoflurane changed the levels of a small number of peptides, primarily degradation products of the hormone somatotropin, but did not influence the levels of most other peptide hormones. Acute use of sodium pentobarbital had negligible impact on the relative abundance of all measured peptides. Overall, our results suggest that anesthetics used in pituitary peptidomics studies do not dramatically confound observed results.

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Section: ■ Results and Discussionmentioning

confidence: 88%

Section: Introductionmentioning

confidence: 99%

Short-Term Administration of Common Anesthetics Does Not Dramatically Change the Endogenous Peptide Profile in the Rat Pituitary

Mousavi

Qiu

Heinis

et al. 2022

ACS Chem. Neurosci.

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“…Neuropeptide Y (NPY), acting through Y1 receptors, regulates the 5-HT system and coordinates aggressive behavior ( Karl et al, 2004 ). Moreover, hippocampal NPY concentrations decrease after sevoflurane treatment ( Kang et al, 2020 ). These results suggest that 5-HT and NPY may be involved in sevoflurane-induced postoperative agitation.…”

Section: Sevoflurane-inhalation Anesthesia and Pocdmentioning

confidence: 99%

Update on the Mechanism and Treatment of Sevoflurane-Induced Postoperative Cognitive Dysfunction

Wang

Chen

Zhang

et al. 2021

Front. Aging Neurosci.

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Sevoflurane is one of the most widely used anesthetics for the induction and maintenance of general anesthesia in surgical patients. Sevoflurane treatment may increase the incidence of postoperative cognitive dysfunction (POCD), and patients with POCD exhibit lower cognitive abilities than before the operation. POCD affects the lives of patients and places an additional burden on patients and their families. Understanding the mechanism of sevoflurane-induced POCD may improve prevention and treatment of POCD. In this paper, we review the diagnosis of POCD, introduce animal models of POCD in clinical research, analyze the possible mechanisms of sevoflurane-induced POCD, and summarize advances in treatment for this condition.

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“…Sevoflurane, a common, inhaled anesthetic used during surgery, has a rapid effect and low airway irritability (Delgado‐Herrera et al, 2001). However, many studies have indicated that exposure to sevoflurane induces neurotoxicity in animal models by regulating apoptosis, which leads to cognitive dysfunction (Kang et al, 2020; Yu et al, 2017; Zhu et al, 2020). In contrast, activation of autophagy has previously been shown to alleviate neurotoxicity and has a protective role on neural cells (Li et al, 2017).…”

Section: Introductionmentioning

confidence: 99%

Echinacoside alleviates sevoflurane‐induced cognitive dysfunction by activating FOXO1‐mediated autophagy

Heng

2022

Intl J of Devlp Neuroscience

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The current study aimed to examine the effects of echinacoside on cognitive impairment in mice after exposure to sevoflurane. To examine the role of FOXO1, si‐FOXO1 and si‐con were injected into the hippocampus through the left lateral cerebral ventricles. Sevoflurane‐induced mice had serious cognitive dysfunction. However, pretreatment with echinacoside alleviated the cognitive dysfunction, as measured by a shortened escape latency time, and increased platform crossing times, the percentage of distance in the target quadrant and Y‐maze spontaneous alternations. In addition, we found that echinacoside elevated FOXO1 expression in the hippocampus; increased the expression of autophagy‐related proteins including Beclin 1, ATG5, ATG7, and LC3; and reduced P62 expression. Silencing of FOXO1 aggravated the cognitive deficits and reduced expression of the autophagy‐related markers, whereas the effects of si‐FOXO1 on memory were abrogated by echinacoside. Echinacoside attenuated the cognitive impairment in sevoflurane‐induced mice through FOXO1‐mediated autophagy.

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Sevoflurane Induces Hippocampal Neuronal Apoptosis by Altering the Level of Neuropeptide Y in Neonatal Rats

Cited by 12 publications

References 41 publications

Short-Term Administration of Common Anesthetics Does Not Dramatically Change the Endogenous Peptide Profile in the Rat Pituitary

Short-Term Administration of Common Anesthetics Does Not Dramatically Change the Endogenous Peptide Profile in the Rat Pituitary

Update on the Mechanism and Treatment of Sevoflurane-Induced Postoperative Cognitive Dysfunction

Echinacoside alleviates sevoflurane‐induced cognitive dysfunction by activating FOXO1‐mediated autophagy

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