Expression of pulmonary vasoactive factors after sevoflurane anaesthesia in rats: a quantitative real-time polymerase chain reaction study

Takemori, Ken; Kobayashi, Katsuya; Sakamoto, Atsuhiro

doi:10.1093/bja/aem347

Cited by 15 publications

(11 citation statements)

References 19 publications

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“…In our previous genomic studies, we administered 4.0% or 4.5% sevoflurane for 6 h and showed that sevoflurane anesthesia affected the expression of many genes and mRNAs in rat lungs (27,31). Here, the reason we experimented with both 2.0% and 4.0% sevoflurane is that inhalation of 4.0% sevoflurane affected circulation (Table 1), and as a result, hypotension, rather than the drug itself, could have affected miRNA expression.…”

Section: Discussionmentioning

confidence: 92%

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Changes in microRNA expression in rat lungs caused by sevoflurane anesthesia: a TaqMan^|^reg; low-density array study

Tanaka¹,

Ishikawa²,

Arai³

et al. 2012

Biomed. Res.

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Reportedly, a large number of microRNAs (miRNAs) play an important role in inflammatory lung diseases such as asthma, idiopathic pulmonary fibrosis (IPF), acute respiratory distress syndrome (ARDS), and pulmonary arterial hypertension (PAH). Sevoflurane is routinely used to various patients, and its safety has been confirmed by clinical outcomes; however, its effects to lungs at the miRNA level have not been elucidated. In our previous genomic studies, we showed that sevoflurane anesthesia affected the expression of many genes and mRNAs in rat lungs. In this study, we comprehensively investigated changes in miRNA expression caused by sevoflurane anesthesia (2.0% and 4.0%). Sevoflurane anesthesia resulted in apparent changes in miRNA expression in rat lungs, and the pattern of 2.0% sevoflurane-induced changes in miRNA expression was similar to that of 4.0% sevoflurane. Some of the differentially expressed miRNAs are known to be involved in asthma, IPF, and PAH. Especially, miR-146a, the most up-regulated miRNA, is known to attenuate the toxic effects associated with LPS stimulation. We showed, for the first time, dynamic changes in miRNA expression caused by sevoflurane anesthesia, and moreover, our results were important to understand the influence of sevoflurane anesthesia on any patients suffered from various lung diseases.

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Section: Discussionmentioning

confidence: 92%

“…In our previous genomic studies, we showed that sevoflurane anesthesia affected the expression of many genes and mRNAs in rat lungs (27,31); therefore, we hypothesized that sevoflurane anesthesia also influences miRNA expression in the lung. Using TaqMan low-density arrays (TLDAs), we investigated sevoflurane-dependent changes in miRNA expression in rat lungs.…”

mentioning

confidence: 93%

Changes in microRNA expression in rat lungs caused by sevoflurane anesthesia: a TaqMan^|^reg; low-density array study

Tanaka¹,

Ishikawa²,

Arai³

et al. 2012

Biomed. Res.

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“…The amplification of NPY and IL-1β was performed in a fast 96-well reaction plate (Applied Biosystems, Foster City, CA, USA), as previously described (25). Reactions were carried out in a 20-µl volume containing 10 µl of TaqMan Universal PCR master mix, 1 µl of TaqMan gene expression assays (Applied Biosystems), 8 µl of RNase-free water (Wako, Tokyo, Japan) and 20 ng of cDNA.…”

Section: Reverse Transcription-quantitative Polymerase Chain Reactionmentioning

confidence: 99%

Effect of electroconvulsive stimulation on messenger RNA expression in the prefrontal cortex in a rat pain model

et al. 2015

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Abstract. Previous reports have shown that electroconvulsive therapy (ECT) is efficacious in the treatment of neuropathic pain; however, its mechanism of action remains unclear. The present study aimed to understand these mechanisms by investigating the alterations in the expression of neuropeptide Y (NPY) and interleukin-1β (IL-1β) in the prefrontal cortex. A rat model of neuropathic pain produced by chronic constrictive injury of the sciatic nerve was used, and mechanical and thermal hyperalgesia were evaluated starting 2 days after the injury. Using a pulse generator, ECT was administered to the rodents for 6 days from days 7-12 after the injury. Thermal and mechanical stimulation were administered to assess pain thresholds. Quantitative polymerase chain reaction, used to measure gene expression levels in the prefrontal cortex, showed that NPY and IL-1β gene expression levels in the prefrontal cortex increased following the injury. The present results indicate that these gene expression level variations may be associated with the mechanisms underlying the effect of ECT in treating neuropathic pain.

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“…A previous study found that HO-1 expression prevents rat livers from ischemia/reperfusion (I/R) injury when using anesthetic sevoflurane (Sevo) clinically (3). Inhalation of Sevo prior to ischemia increases the activity of HO-1 in the lung and protects from lung I/R injury in rats (4). I/R injury is an important model of oxidant-mediated ALI (5).…”

Section: Introductionmentioning

confidence: 99%

Post-conditioning with sevoflurane induces heme oxygenase-1 expression via the PI3K/Akt pathway in lipopolysaccharide-induced acute lung injury

Zhao

Wu²,

Zhang

et al. 2014

Molecular Medicine Reports

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Abstract. The aim of the present study was to explore the regulatory mechanism of heme oxygenase-1 (HO-1) expression induced by sevoflurane (Sevo) in lipopolysaccharide (LPS)-induced acute lung injury (ALI). Sprague-Dawley rats were divided randomly into six groups: (A) Control, (B) 2.4% Sevo only, (C) LY294002 (PI3K inhibitor) only, (D) LPS + 2.4% Sevo, (E) LY294002 + LPS + 2.4% Sevo and (F) LPS only. The pathological changes in wet/dry weight ratio (W/D), the activities of superoxide dismutase, myeloperoxidase (MPO), malondialdehyde, and HO-1, as well as the expression of intercellular adhesion molecule (ICAM-1), HO-1, phospho-phosphatidylinositol 3-kinase (pPI3K) and phospho-Akt (pAkt) were recorded. Sevo post-conditioning was able to effectively protect from ALI with decreasing pathomorphological scores, MPO activity, W/D and the mRNA and protein expression levels of ICAM-1. Sevo promotes HO-1 expression via the PI3K/protein kinase B (PI3K/Akt) pathway with activation of pPI3K and pAkt. Inhibition of the PI3K/Akt pathway by LY294002 partly eliminates the protective effects of Sevo. It is concluded that Sevo post-conditioning has a vital role in inducing the upregulation of HO-1 expression via the PI3K/Akt pathway to alleviate ALI.

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Expression of pulmonary vasoactive factors after sevoflurane anaesthesia in rats: a quantitative real-time polymerase chain reaction study

Abstract: Sevoflurane increased the expressions of ET-1, NOS3, and ADM. Our results suggest that the increased expressions of NOS3 and ADM may counteract that of ET-1 and so regulate pulmonary circulation under sevoflurane anaesthesia.

Cited by 15 publications

References 19 publications

Changes in microRNA expression in rat lungs caused by sevoflurane anesthesia: a TaqMan^|^reg; low-density array study

Changes in microRNA expression in rat lungs caused by sevoflurane anesthesia: a TaqMan^|^reg; low-density array study

Effect of electroconvulsive stimulation on messenger RNA expression in the prefrontal cortex in a rat pain model

Post-conditioning with sevoflurane induces heme oxygenase-1 expression via the PI3K/Akt pathway in lipopolysaccharide-induced acute lung injury

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