&lt;b&gt;Influence of neonatal sevoflurane exposure on nerve development-related microRNAs and behavior of &lt;/b&gt;&lt;b&gt;rats &lt;/b&gt;

Fujimoto, Saiko; Ishikawa, Masashi; Nagano, Masatoshi; Sakamoto, Atsuhiro

doi:10.2220/biomedres.36.347

Cited by 15 publications

(8 citation statements)

References 28 publications

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“…For example, Fujimoto et al . () reported changes in a number of nerve development‐related microRNAs, including rno‐miRNA‐632, mmu‐miR‐211 and mmu‐miR‐872, in the hippocampus of neonatal rats in response to sevoflurane exposure, leading to subsequent behavioural disorders. Lu et al .…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‐27a‐3p suppression of peroxisome proliferator‐activated receptor‐γ contributes to cognitive impairments resulting from sevoflurane treatment

Jia

Jiang

et al. 2017

Journal of Neurochemistry

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Sevoflurane is the most widely used anaesthetic administered by inhalation. Exposure to sevoflurane in neonatal mice can induce learning deficits and abnormal social behaviours. MicroRNA (miR)-27a-3p, a short, non-coding RNA that functions as a tumour suppressor, is up-regulated after inhalation of anaesthetic, and peroxisome proliferator-activated receptor γ (PPAR-γ) is one of its target genes. The objective of this study was to investigate how the miR-27a-3p-PPAR-γ interaction affects sevoflurane-induced neurotoxicity. A luciferase reporter assay was employed to identify the interaction between miR-27a-3p and PPAR-γ. Primary hippocampal neuron cultures prepared from embryonic day 0 C57BL/6 mice were treated with miR-27a-3p inhibitor or a PPAR-γ agonist to determine the effect of miR-27a-3p and PPAR-γ on sevoflurane-induced cellular damage. Cellular damage was assessed by a flow cytometry assay to detect apoptotic cells, immunofluorescence to detect reactive oxygen species, western blotting to detect NADPH oxidase 1/4 and ELISA to measure inflammatory cytokine levels. In vivo experiments were performed using a sevoflurane-induced anaesthetic mouse model to analyse the effects of miR-27a-3p on neurotoxicity by measuring the number of apoptotic neurons using the Terminal-deoxynucleoitidyl Transferase Mediated Nick End Labeling (TUNEL) method and learning and memory function by employing the Morris water maze test. Our results revealed that PPAR-γ expression was down-regulated by miR-27a-3p following sevoflurane treatment in hippocampal neurons. Down-regulation of miR-27a-3p expression decreased sevoflurane-induced hippocampal neuron apoptosis by decreasing inflammation and oxidative stress-related protein expression through the up-regulation of PPAR-γ. In vivo tests further confirmed that inhibition of miR-27a-3p expression attenuated sevoflurane-induced neuronal apoptosis and learning and memory impairment. Our findings suggest that down-regulation of miR-27a-3p expression ameliorated sevoflurane-induced neurotoxicity and learning and memory impairment through the PPAR-γ signalling pathway. MicroRNA-27a-3p may, therefore, be a potential therapeutic target for preventing or treating sevoflurane-induced neurotoxicity.

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Section: Discussionmentioning

confidence: 99%

MicroRNA‐27a‐3p suppression of peroxisome proliferator‐activated receptor‐γ contributes to cognitive impairments resulting from sevoflurane treatment

Jia

Jiang

et al. 2017

Journal of Neurochemistry

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“…These studies revealed that IGF-1 was an important factor to perfume sevoflurane Accumulating evidence has proven that the differential expression of miRNAs is induced by sevoflurane treatment. For instance, the exposure to sevoflurane during early neural development alters hippocampus-related miRNA expression thus inducing behavioral disorders (Fujimoto, Ishikawa, Nagano, & Sakamoto, 2015). MiR-125b and miR-181a were up-regulated in rat hippocampus treated with sevoflurane (Goto, Hori, Ishikawa, Tanaka, & Sakamoto, 2014).…”

Section: Igf-1 Inhibited the Positive Effect Of Sevoflurane On Tissue Necrosis And Apoptosismentioning

confidence: 99%

Sevoflurane induces liver injury by modulating the expression of insulin‐like growth factor 1 via miR‐214

Zhao

Xie

2018

Journal Cellular Physiology

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This study aimed to detect the effect of sevoflurane anesthesia on liver injury through modulating IGF-1. The expression of IGF-1 and IGF-1R in liver tissues of sevoflurane-exposed rats was examined by qRT-PCR and Western blot. The expression levels of miR-214 in liver cells treated with different concentration of sevoflurane at different time points were detected by qRT-PCR. Enzyme-linked immunosorbent (ELISA) assay was used to analyze serum IGF-1 concentration in cell culture media. After pre-treatment with 100 nM miR-214 inhibitor followed by exposure to sevoflurane, the expression level of miR-214 and IGF-1 protein in liver cells was examined. Hematoxylin-Eosin (HE) staining and TUNEL assay was performed to analyze liver tissue necrosis and apoptosis. The expression levels of apoptosis-related proteins (caspase 3 and Bcl-xL) were examined using Western blot. The mRNA and protein expression level of IGF-1 and IGF-1R in rats was significantly down-regulated after 90 min exposure to sevoflurane. QRT-PCR results suggested that exposure to sevoflurane upregulated the expression level of miR-214 and decreased the concentration of IGF-1 in a dose and time dependent manner. Sevoflurane inhibited the expression of IGF-1 through up-regulating miR-214. IGF-1 inhibited the positive effect of sevoflurane on cell necrosis and apoptosis. Sevoflurane could induce liver injury by modulating IGF-1 expression via miR-214.

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“…To date, the molecular mechanisms underlying sevoflurane-induced neurotoxicity have not been fully elucidated. However, a number of studies have demonstrated that exposure to sevoflurane induces alterations in the microRNA (miR) expression profile (10)(11)(12)(13)(14).…”

Section: Introductionmentioning

confidence: 99%

Sevoflurane‑induced neurotoxicity is driven by OXR1 post‑transcriptional downregulation involving hsa‑miR‑302e

et al. 2018

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Sevoflurane is a common anesthetic agent used in surgical settings and previous studies have indicated that it exerts a neurotoxic effect. However, the molecular mechanism underlying this side effect is unknown. In addition, the human microRNA‑302 (hsa‑miR‑302) family members have been reported to be involved in neuronal cell development and biology. Thus, the present study aimed to investigate the potential implication of hsa‑miR‑302e in the sevoflurane‑induced cytotoxicity on human hippocampal cells (HN‑h). HN‑h cells were transfected with hsa‑miR‑302e mimic, hsa‑miR‑302e inhibitor or negative controls and subsequently exposed to different concentrations of sevoflurane. An MTT assay was used to assess the cytotoxicity of sevoflurane on HN‑h cells. Cell apoptosis was determined by flow cytometry. The levels of lactate dehydrogenase release, reactive oxygen species, lipid peroxidation and intracellular calcium (Ca2+) were additionally detected. Reverse transcription‑quantitative polymerase chain reaction and western blotting were conducted to determine mRNA and protein expression, respectively. A luciferase assay was performed for validating the targeting of OXR1 by hsa‑miR‑302e. The results indicated that sevoflurane induced a decrease in cell viability, malondialdehyde and reactive oxygen species production, lactate dehydrogenase release, intracellular Ca2+ production, calcium/calmodulin‑dependent protein kinase II phosphorylation and apoptosis. In addition, treatment with sevoflurane induced the expression of hsa‑miR‑302e while the expression of its target, oxidation resistance gene 1 (OXR1), was significantly downregulated. Inhibition of hsa‑miR‑302e expression protected neuronal cells from sevoflurane cytotoxicity. Mechanistic studies demonstrated that OXR1 was a direct target of hsa‑miR‑302e. Furthermore, the overexpression of OXR1 abolished the effect of sevoflurane on neuronal cells. The results of the present study indicated that sevoflurane exerts its neurotoxic effect by regulating the hsa‑miR‑302e/OXR1 axis. Therefore, the manipulation of the hsa‑miR‑302e/OXR1 pathway will be useful for preventing sevoflurane‑induced neurotoxicity.

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<b>Influence of neonatal sevoflurane exposure on nerve development-related microRNAs and behavior of </b><b>rats </b>

Cited by 15 publications

References 28 publications

MicroRNA‐27a‐3p suppression of peroxisome proliferator‐activated receptor‐γ contributes to cognitive impairments resulting from sevoflurane treatment

MicroRNA‐27a‐3p suppression of peroxisome proliferator‐activated receptor‐γ contributes to cognitive impairments resulting from sevoflurane treatment

Sevoflurane induces liver injury by modulating the expression of insulin‐like growth factor 1 via miR‐214

Sevoflurane‑induced neurotoxicity is driven by OXR1 post‑transcriptional downregulation involving hsa‑miR‑302e

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