Postoperative Cognitive Effects in Newborns

Zuo, Zhiyi

doi:10.1097/aln.0b013e3182835276

Cited by 6 publications

(4 citation statements)

References 21 publications

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“…Neuroinflammation has been suggested to play a critical role in the development of POCD [ 4 ]. Clinical and experimental evidence has shown that anti-inflammation treatment could reduce POCD [ 5 – 7 ]. Age-related inflammation is characterized by a chronic mild inflammation called “inflammaging” [ 1 , 8 ], which negatively impacts central nervous system (CNS) function [ 9 ].…”

Section: Introductionmentioning

confidence: 99%

Critical role of NLRP3-caspase-1 pathway in age-dependent isoflurane-induced microglial inflammatory response and cognitive impairment

Wang

Meng

Cao

et al. 2018

J Neuroinflammation

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165

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BackgroundElderly patients are more likely to suffer from postoperative cognitive dysfunction (POCD) after surgery and anesthesia. Except for declined organ function, the particular pathogenesis of POCD in elderly patients remains unknown. This study is carried out to determine the critical role of the NOD-like receptor protein 3 (NLRP3)-caspase-1 pathway in isoflurane-induced cognitive impairment.MethodsYoung (6–8 months old) and aged (14 months old) healthy male C57BL/6 mice were exposed to 1.5% isoflurane for 2 h. Some mice received intraperitoneal injection of Ac-YVAD-cmk (8 mg/kg), a specific inhibitor of caspase-1, 30 min before the isoflurane exposure. Morris water maze test was carried out 1 week after the isoflurane anesthesia. Brain tissues were harvested 24 h after the isoflurane anesthesia. Western blotting was carried out to detect the expression of NLRP3, interleukin (IL)-1β, and IL-18 in the hippocampus. Mouse microglial cell line BV-2 and primary microglial cultures were primed by lipopolysaccharide for 30 min before being exposed to isoflurane. NLRP3 was downregulated by RNA interference.ResultsCompared to young mice, aged mice had an increased expression of NLRP3 in the hippocampus. Isoflurane induced cognitive impairment and hippocampal inflammation in aged mice but not in young mice. These effects were attenuated by Ac-YVAD-cmk pretreatment (P < 0.05). Isoflurane activated NLRP3-caspase-1 pathway and increased the secretion of IL-18 and IL-1β in cells pretreated with lipopolysaccharide but not in cells without pretreatment. Downregulation of NLRP3 attenuated the activation of NLRP3 inflammasome by isoflurane.ConclusionsNLRP3 priming status in aged mouse brain may be involved in isoflurane-induced hippocampal inflammation and cognitive impairment.Electronic supplementary materialThe online version of this article (10.1186/s12974-018-1137-1) contains supplementary material, which is available to authorized users.

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Section: Introductionmentioning

confidence: 99%

Critical role of NLRP3-caspase-1 pathway in age-dependent isoflurane-induced microglial inflammatory response and cognitive impairment

Wang

Meng

Cao

et al. 2018

J Neuroinflammation

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165

158

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“…In addition, neuroapoptosis, neuroinflammation, and oxidative stress have been demonstrated to be the important etiological factors in the development of POCD (Brambrink et al, 2010; Wu et al, 2012). Animal studies have suggested an increased inflammatory cytokines induction by anesthesia in the brain after surgery (Wang et al, 2018), and ISO‐induced cognitive dysfunction can be ameliorated by suppressing neuroinflammation (Zhang, Li, Li, Hou, & Hou, 2016; Zuo, 2013). In addition, ISO exposure can induce oxidative stress in the brain leading to initiation of neuron apoptosis and subsequently cognitive impairment (Shao, Wu, Bai, Fu, & Zou, 2019; Shen, Shang, Wu, & Ren, 2020).…”

Section: Introductionmentioning

confidence: 99%

Protective effects of chlorogenic acid on isoflurane‐induced cognitive impairment of aged mice

Chong

Yang

Zhou

et al. 2022

Food Science & Nutrition

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Postoperative cognitive dysfunction (POCD) is characterized by impairment in cognitive functions in patients following anesthesia and surgery. Chlorogenic acid (CGA) is a plant‐derived compound possessing numerous bioactive properties. The aim of this study was to investigate the therapeutic potential of CGA in isoflurane (ISO)‐induced cognitive dysfunction of aged mice, and further identify the mechanisms involved in the protective effects of CGA. A total of 80 male C57BL/6 mice, 20‐month‐old, were randomly divided into control group, isoflurane group (ISO), and ISO + 30 mg/kg CGA group and ISO + 60 mg/kg CGA. CGA was given orally once daily for 7 days to the mice and they were exposed to ISO (1.5%; 4 h). The open‐field and Morris water maze tests were used to investigate the cognitive function of mice. Pretreatment with CGA significantly attenuated ISO‐induced cognitive impairment. The levels of IL‐1β, TNF‐α, IL‐6, nuclear p65 NF‐kB, cleaved caspase‐3, and Bax were significantly increased, while the levels of IkBα and Bcl‐2 were decreased in the hippocampus 24 h after the ISO anesthesia. All the mentioned effects induced by ISO were reversed by CGA pretreatment. Furthermore, ISO exposure induced marked downregulation of SOD, CAT, HO‐1, and NQO‐1 and elevation of MDA and nuclear translocation of Nrf2 in the hippocampus tissue. All these parameters were reversed by CGA treatment. Importantly, the higher dose of CGA (60 mg/kg) showed a greater neuroprotective effect. In conclusion, these findings suggest that CGA attenuates the ISO‐induced cognitive impairment via its anti‐inflammatory, anti‐oxidative, and anti‐apoptotic properties in aged mice.

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“…2 Neuroinflammation has been reported to participate in cognitive impairment associated with some neurodegenerative diseases, and clinical as well as experimental evidence has shown that anti-inflammation treatment could alleviate cognitive impairment. [3][4][5] The common characteristic of these diseases is progressive neuronal loss and impaired neuronal function, lacking effective treatments. 6 Lipopolysaccharide (LPS), a major component of various gram-negative bacteria, has been shown to induce hippocampal neuroinflammation and cognitive decline, is generally utilized to activate inflammation and prepared cognitive impairment model in vitro or in vivo.…”

Section: Introductionmentioning

confidence: 99%

“…PD, AD and PND. [3][4][5] Studies have indicated that LPSinduced neuroinflammation models are valid for deciphering the mechanism underlying neurodegeneration and cognitive impairment. [39][40][41][42] The MWM test and Y-maze test, the most common behavioral tools in neuroscience, were used as reliable tests that reflect hippocampaldependent learning and memory in laboratory animals.…”

mentioning

confidence: 99%

MicroRNA-138-5p Regulates Hippocampal Neuroinflammation and Cognitive Impairment by NLRP3/Caspase-1 Signaling Pathway in Rats

Feng

Zhan

et al. 2021

JIR

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Purpose Neuroinflammation is an essential causative factor in the pathogenesis and progression of cognitive impairment. The present study aims to evaluate the critical role of microRNA-138-5p (miR-138-5p) in hippocampal neuroinflammation and cognitive impairment through the NLRP3/caspase-1 signaling pathway in rats. Material and Methods We established the cognitive impairment rat model and RM (Rat microglia) microglial cellular inflammation model by intracerebroventricular (icv) injection or stimulation of lipopolysaccharide (LPS). Morris water maze (MWM) and Y-maze tests were performed to assess the cognitive behaviors. Quantitative real-time polymerase chain reaction (qRT-PCR), Enzyme-linked immune-sorbent assay (ELISA) and Western blot analysis were utilized to evaluate mRNA or protein expression. Bioinformatic analysis and dual-luciferase reporter gene assay were performed to verify the targeting relationship between NLRP3 and miR-138-5p. Besides, Hematoxylin and eosin (H&E) staining and immunohistochemistry were applied to observe the neuronal morphology and detect the positive cells of the hippocampus, respectively. Results Compared to the control groups, LPS-treated rats exhibited significantly impaired learning and memory in MWM and Y-maze tests. The expression of NLRP3, caspase-1 and pro-inflammation cytokines (IL-1β and IL-18) were upregulated, while miR-138-5p was downregulated both in rat hippocampus and RM cells treated with LPS. MiR-138-5p is downregulated in microarray data of cognitive impairment animals and could directly target the 3ʹ-UTR of NLRP3. Furthermore, upregulation of miR-138-5p improved impaired cognitive functions, while inhibited hippocampal neuroinflammation demonstrated by decreased expression of NLRP3/caspase-1 axis, pro-inflammation cytokines and microglial activation. This study demonstrates for the first time that miR-138-5p suppresses the hippocampal NLRP3/caspase-1 signaling pathway activation in cognition impaired rats. Conclusion The low expression of miR-138-5p after LPS administration may contribute to the activation of the NLRP3/caspase-1 pathway, leading to hippocampal neuroinflammation and cognitive impairment in rat models. These findings indicate a promising therapeutic avenue for cognitive disorders.

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Postoperative Cognitive Effects in Newborns

Cited by 6 publications

References 21 publications

Critical role of NLRP3-caspase-1 pathway in age-dependent isoflurane-induced microglial inflammatory response and cognitive impairment

Critical role of NLRP3-caspase-1 pathway in age-dependent isoflurane-induced microglial inflammatory response and cognitive impairment

Protective effects of chlorogenic acid on isoflurane‐induced cognitive impairment of aged mice

MicroRNA-138-5p Regulates Hippocampal Neuroinflammation and Cognitive Impairment by NLRP3/Caspase-1 Signaling Pathway in Rats

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