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Sevoflurane induced neurotoxicity

Bin Liu, Junming Xia, Yali Chen, Jun Zhang
Neonatal exposure to volatile anesthetics causes apoptotic neurodegeneration in the developing brain, possibly leading to neurocognitive deficits in adulthood. Endoplasmic reticulum (ER) stress might be associated with sevoflurane (sevo)-induced neuroapoptosis. However, the signaling pathway regulating sevo-induced neuroapoptosis is not understood. We investigated the effects of neonatal sevo exposure on ER signaling pathway activation. Seven-day-old mouse pups were divided into control (C) and sevo (S; 3 % sevo exposure, 6 h) groups...
September 28, 2016: Neurotoxicity Research
Guorong Tao, Yan Luo, Qingsheng Xue, Guohui Li, Yongchang Tan, Jinglei Xiao, Buwei Yu
Sevoflurane exposures were demonstrated to induce neurotoxicity in the developing brain in both human and animal studies. However, there is no effective approach to reverse it. The present study aimed to evaluate the feasibility of utilizing docosahexaenoic acid (DHA) to prevent sevoflurane-induced neurotoxicity. P6 (postnatal 6 days) mice were administrated DHA after exposure to 3% sevoflurane for two hours daily in three consecutive days. Molecular expressions of synaptic makers (PSD95, synaptophysin) and synaptic morphological changes were investigated by Western blot analysis and transmission electron microscopy, respectively...
2016: BioMed Research International
Jishi Ye, Zongze Zhang, Yanlin Wang, Chang Chen, Xing Xu, Hui Yu, Mian Peng
Although accumulating evidence has suggested that microRNAs (miRNAs) have a serious impact on cognitive function and are associated with the etiology of several neuropsychiatric disorders, their expression in sevoflurane-induced neurotoxicity in the developing brain has not been characterized. In the present study, the miRNAs expression pattern in neonatal hippocampus samples (24 h after sevoflurane exposure) was investigated and 9 miRNAs were selected, which were associated with brain development and cognition in order to perform a bioinformatic analysis...
September 2016: Experimental and Therapeutic Medicine
Li-Yan Wang, Zhi-Jun Tang, Yu-Zeng Han
Millions of infants and children are exposed to anesthesia every year during medical care. Sevoflurane is a volatile anesthetic that is frequently used for pediatric anesthesia. However, previous reports have suggested that the administration of sevoflurane promotes neurodegeneration, raising concerns regarding the safety of its usage. The present study aimed to investigate caffeic acid phenethyl ester (CAPE) and its protective effect against sevoflurane‑induced neurotoxicity in neonatal rats. Rat pups were administered with CAPE at 10, 20 or 40 mg/kg body weight from postnatal day 1 (P1) to P15...
October 2016: Molecular Medicine Reports
Jeffrey H Zimering, Yuanlin Dong, Fang Fang, Lining Huang, Yiying Zhang, Zhongcong Xie
Early postnatal anesthesia causes long-lasting learning and memory impairment in rodents, however, evidence for a specific neurotoxic effect on early synaptogenesis has not been demonstrated. Drebrin A is an actin binding protein whose localization in dendritic protrusions serves an important role in dendritic spine morphogenesis, and is a marker for early synaptogenesis. We therefore set out to investigate whether clinically-relevant concentrations of anesthetic sevoflurane, widely- used in infants and children, alters dendritic morphology in cultured fetal day 16 mouse hippocampal neurons...
2016: PloS One
Xiaohui Chen, Xue Zhou, Dihan Lu, Xiaoyu Yang, Zhibin Zhou, Xi Chen, Yanqing Chen, Wen He, Xia Feng
The commonly used volatile anesthetic sevoflurane has been shown to induce widespread apoptosis in the developing brain, yet the underlying molecular mechanisms are not fully understood. Accumulating research has demonstrated that long noncoding RNAs (lncRNAs) regulate multiple biological processes, including neural development, differentiation and apoptosis. They are aberrantly expressed in multiple neurodegenerative diseases. In this study, we employed a lncRNA-mRNA microarray analysis to determine whether and how lncRNAs are involved in sevoflurane-induced hippocampal neuronal apoptosis in neonatal mice...
October 2016: Metabolic Brain Disease
Xuan Zhang, Shuliang Liu, Glenn D Newport, Merle G Paule, Ralph Callicott, James Thompson, Fang Liu, Tucker A Patterson, Marc S Berridge, Scott M Apana, Christina C Brown, Mackean P Maisha, Joseph P Hanig, William Slikker, Cheng Wang
BACKGROUND: Animals exposed to sevoflurane during development sustain neuronal cell death in their developing brains. In vivo micro-positron emission tomography (PET)/computed tomography imaging has been utilized as a minimally invasive method to detect anesthetic-induced neuronal adverse effects in animal studies. METHODS: Neonatal rhesus monkeys (postnatal day 5 or 6, 3 to 6 per group) were exposed for 8 h to 2.5% sevoflurane with or without acetyl-L-carnitine (ALC)...
July 2016: Anesthesiology
Z Sun, M Satomoto, Y U Adachi, H Kinoshita, K Makita
BACKGROUND: Neonatal exposure to anaesthetics such as sevoflurane has been reported to result in behavioural deficits in rodents. However, while oxidative injury is thought to play an underlying pathological role, the mechanisms of neurotoxicity remain unclear. In the present study, we investigated whether the NADPH oxidase inhibitor apocynin protects against long-term memory impairment produced by neonatal sevoflurane exposure in mice. METHODS: Postnatal day six mice were divided into four groups; (1) non-anaesthesia, (2) intraperitoneal apocynin (50 mg kg(-1)) treatment, (3) 3% sevoflurane exposure for 6 h, and (4) apocynin treatment combined with sevoflurane exposure...
July 2016: British Journal of Anaesthesia
Choon L Bong, Angela S H Yeo, Teddy Fabila, Josephine S K Tan
BACKGROUND: Recent concerns regarding possible long-term effects of early anesthesia exposure on neurodevelopment in children have provided an impetus to explore alternative anesthetic techniques using potentially neuroprotective agents. Dexmedetomidine has not been implicated in anesthesia-induced neurotoxicity and has been shown to be neuroprotective in preclinical studies. We describe a case series of 50 neonates and infants who received dexmedetomidine sedation with caudal anesthesia instead of general endotracheal anesthesia for inguinal hernia surgery...
June 2016: Paediatric Anaesthesia
You-Fa Zhou, Qing-Xia Wang, Hai-Yan Zhou, Gang Chen
AIM: The inhaled anesthetic sevoflurane may induce cognitive impairment in both animals and humans. Previous study has shown that sevoflurane triggers ER stress and may lead to apoptosis in rat hippocampal neurons. In this study, we examined whether sevoflurane caused autophagy and its contributions to sevoflurane induced neuronal cell injury. METHODS: H4 human neuroglioma cells were exposed to 4.1% sevoflurane for 6 h. Cell viability and apoptosis ratio were assessed using a CCK8 kit and flow cytometry, respectively...
May 2016: Acta Pharmacologica Sinica
Fenglian Xu, Ryden Armstrong, Daniela Urrego, Munir Qazzaz, Mario Pehar, J N Armstrong, Tim Shutt, Naweed Syed
BACKGROUND: Concerns have risen regarding the potential side effects of clinical exposure of the pediatric population to inhalational anesthetics, and how they might impact cognitive, learning, and memory functions. However, neither the mechanisms of anesthetic cytotoxicity, nor potential protective strategies, have yet been fully explored. In this study, we examined whether two of the most commonly used inhalational anesthetics, sevoflurane and desflurane, affect neuronal viability and synaptic network assembly between cultured rat cortical neurons...
2016: Molecular Brain
Wei Wang, Rui Lu, Da-Yun Feng, Hui Zhang
BACKGROUND: The mechanisms underlying general anesthesia-induced neurotoxicity are unclear. Astrocytes have been recognized as important contributors to neuronal development. Until now, the response of the astrocytes to neonatal general anesthetic exposure has been unreported. METHODS: Postnatal day 7 rats received 2.5% sevoflurane for 6 hours. Expressions of glial fibrillary acidic protein (GFAP) and glutamate-aspartate transporter (GLAST) and phosphorylation of the Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway were detected on days 1, 3, 7, and 14 after sevoflurane inhalation...
July 2016: Anesthesia and Analgesia
Q Song, Y L Ma, J Q Song, Q Chen, G S Xia, J Y Ma, F Feng, X J Fei, Q M Wang
Sevoflurane, the most widely used anesthetic in clinical practice, has been shown to induce apoptosis, inhibit neurogenesis, and cause learning and memory impairment in young mice. However, the underlying mechanism is still unknown. In this study, wild-type and the FAS- or FAS ligand (FASL)-knockout mice (age 7 days) were exposed to sevoflurane or pure oxygen. Western blotting was used to examine the expression of FAS protein. Terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) and bromodeoxyuridine (BrdU) staining were employed to quantify the apoptotic cells and newborn cells in the hippocampus and Morris water maze (MWM) in order to evaluate learning and memory status...
December 22, 2015: Genetics and Molecular Research: GMR
W-Y Wang, X-M Wu, L-J Jia, H-H Zhang, F Cai, H Mao, W-C Xu, L Chen, J Zhang, S-F Hu
Beta-arrestins (β-arrs) are initially known as negative regulators of G protein-coupled receptors (GPCRs). Recently, there is increasing evidence suggesting that β-arrs also serve as scaffolds and adapters that mediate distinct intracellular signal transduction initiated by GPCR activation. In the previous study, we have shown that metabotropic glutamate receptor 7 (mGluR7) and extracellular signal-regulated kinase 1 and 2 (ERK1/2) signaling may be involved in the developmental sevoflurane neurotoxicity. In the present study, we showed that activation of mGluR7 with a group III mGluRs orthosteric agonist LAP4 or an atypical mGluR7 allosteric agonist N,N'-bis(diphenylmethyl)-1,2-ethanediamine dihydrochloride (AMN082) significantly attenuated sevoflurane-induced neuronal apoptosis...
January 28, 2016: Neuroscience
Yi-Gang Man, Rui-Gang Zhou, Bing Zhao
Sevoflurane and propofol are widely used in pediatric anesthesia. Neurotoxicity of sevoflurane and propofol in developing brain has been reported and these effects raise concerns on the usage of the drugs. We investigated the influence of rutin, a flavonoid on the neurodegenerative effects of sevoflurane and propofol and on memory and cognition in neonatal rodent model. Separate groups of neonatal mice (C57BL/6) were administered with rutin at 25 or 50 mg/kg body weight (b.wt) from post natal day 2 (P1) to P21...
2015: International Journal of Clinical and Experimental Medicine
Kai-Xiang Xu, Jun Tao, Nan Zhang, Jian-Zhong Wang
Obesity has been reported to be one of the significant contributors to various chronic disease conditions. Childhood obesity has been on an alarming increase over recent years leading to various health complications. Millions of children undergo surgery each year as a part of medical care on various health grounds. In the present study, influence of vitamin C on the effect of obesity and over-weight under anaesthetic exposure was analysed. Separate groups of neonatal mice (C57BL/6) were fed on high-fat diet to induce obesity...
2015: International Journal of Clinical and Experimental Medicine
Yupeng Zhao, Kaizheng Chen, Xia Shen
Sevoflurane is the most widely used inhaled anesthetic. Environmental enrichment (EE) can reverse sevoflurane-induced learning and memory impairment in young mice. However, the mechanism by which EE elicits this effect is unclear. The peroxisome proliferator-activated receptor (PPAR) regulatory pathway plays a critical role in the regulation of inflammation in central nervous system diseases. In this study, we investigated whether EE attenuates sevoflurane-induced learning and memory disability via the PPAR signaling pathway...
2015: BioMed Research International
Fang Liu, Shuo W Rainosek, Jessica L Frisch-Daiello, Tucker A Patterson, Merle G Paule, William Slikker, Cheng Wang, Xianlin Han
Sevoflurane is a volatile anesthetic that has been widely used in general anesthesia, yet its safety in pediatric use is a public concern. This study sought to evaluate whether prolonged exposure of infant monkeys to a clinically relevant concentration of sevoflurane is associated with any adverse effects on the developing brain. Infant monkeys were exposed to 2.5% sevoflurane for 9 h, and frontal cortical tissues were harvested for DNA microarray, lipidomics, Luminex protein, and histological assays. DNA microarray analysis showed that sevoflurane exposure resulted in a broad identification of differentially expressed genes (DEGs) in the monkey brain...
October 2015: Toxicological Sciences: An Official Journal of the Society of Toxicology
Rany Makaryus, Hedok Lee, Tian Feng, June-Hee Park, Maiken Nedergaard, Zvi Jacob, Grigori Enikolopov, Helene Benveniste
BACKGROUND: A wealth of data shows neuronal demise after general anesthesia in the very young rodent brain. Herein, the authors apply proton magnetic resonance spectroscopy (1HMRS), testing the hypothesis that neurotoxic exposure during peak synaptogenesis can be tracked via changes in neuronal metabolites. METHODS: 1HMRS spectra were acquired in the brain (thalamus) of neonatal rat pups 24 and 48 h after sevoflurane exposure on postnatal day (PND) 7 and 15 and in unexposed, sham controls...
September 2015: Anesthesiology
Tao Han, Zhonghua Hu, Yongzhong Tang, Alisha Shrestha, Wen Ouyang, Qin Liao
The aim of the present study was to investigate the roles of Rho protein A (RhoA) and Rho kinases 2 (ROCK2) in the memory dysfunction of adult rats exposed to sevoflurane at postnatal days 7-9 (P7-9). One-week-old Sprague-Dawley rats were divided into four groups known as C, S1, S3 and F. Rats in the S1 (2 h at P7) and S3 groups (2 h/day at P7-9) were exposed to sevoflurane. The rats in the F group were treated with the ROCK2 inhibitor and subsequent sevoflurane exposure (2 h/day at P7-9). The rats in the C group received no sevoflurane...
May 2015: Biomedical Reports
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