Remifentanil attenuates sepsis-induced intestinal injury by inducing autophagy

Remifentanil (RFT), extensively used for general anesthesia, is a synthetic ultra-short-acting opioid used as an anti-inflammatory oxidant to alleviate a plethora of diseases. This study was designed to determine whether RFT would provide protective effects on sepsis-induced intestinal injury. RFT w...

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Autores principales: Mingli Wang, Shiqi Guo, Yu Zhang, Yao Zhang, Hong Zhang
Formato: article
Lenguaje:EN
Publicado: Taylor & Francis Group 2021
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Acceso en línea:https://doaj.org/article/8fc418efd67941af9e0519f3610caac2
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spelling oai:doaj.org-article:8fc418efd67941af9e0519f3610caac22021-11-04T15:51:54ZRemifentanil attenuates sepsis-induced intestinal injury by inducing autophagy2165-59792165-598710.1080/21655979.2021.1997562https://doaj.org/article/8fc418efd67941af9e0519f3610caac22021-10-01T00:00:00Zhttp://dx.doi.org/10.1080/21655979.2021.1997562https://doaj.org/toc/2165-5979https://doaj.org/toc/2165-5987Remifentanil (RFT), extensively used for general anesthesia, is a synthetic ultra-short-acting opioid used as an anti-inflammatory oxidant to alleviate a plethora of diseases. This study was designed to determine whether RFT would provide protective effects on sepsis-induced intestinal injury. RFT was used to incubate the lipopolysaccharide (LPS)-treated IEC-6 cells for determining the role of RFT in sepsis-induced intestinal injury and the underlying mechanism. The determination of cell viability and inflammation of LPS-treated IEC-6 cells influenced by RFT was conducted by Cell counting Kit-8 (CCK-8), RT-qPCR, and western blot, while the detection of LDH, diamine oxidase (DAO), and intestinal-type fatty acid binding proteins (I-FABP) was conducted for determining the intestinal cytotoxicity in these cells. The apoptosis of these cells was detected by TUNEL, with autophagy-related protein expression measured by western blot to confirm whether autophagy was activated. Finally, the aforementioned assays were conducted again after 3-Methyladenine (3-MA), an autophagy inhibitor, was used on these cells to investigate whether RFT exerted its effects on LPS-treated IEC-6 cells via modulation of autophagy. RFT alleviates LPS-induced IEC-6 cell inflammation, cytotoxicity and apoptosis, and autophagy-related proteins were expressed at higher levels when RFT was used on these cells. Nevertheless, further treatment of 3-MA weakened the restorative impacts of RFT on the inflammation, cytotoxicity and apoptosis of these cells. To conclude, this paper is the first to present evidence that RFT attenuates sepsis-induced intestinal injury by inducing autophagy, which will provide instructions for the future investigations into the use of RFT in treatment of intestinal injury.Mingli WangShiqi GuoYu ZhangYao ZhangHong ZhangTaylor & Francis Grouparticleremifentanilsepsis-induced intestinal injuryautophagyBiotechnologyTP248.13-248.65ENBioengineered, Vol 0, Iss 0 (2021)
institution DOAJ
collection DOAJ
language EN
topic remifentanil
sepsis-induced intestinal injury
autophagy
Biotechnology
TP248.13-248.65
spellingShingle remifentanil
sepsis-induced intestinal injury
autophagy
Biotechnology
TP248.13-248.65
Mingli Wang
Shiqi Guo
Yu Zhang
Yao Zhang
Hong Zhang
Remifentanil attenuates sepsis-induced intestinal injury by inducing autophagy
description Remifentanil (RFT), extensively used for general anesthesia, is a synthetic ultra-short-acting opioid used as an anti-inflammatory oxidant to alleviate a plethora of diseases. This study was designed to determine whether RFT would provide protective effects on sepsis-induced intestinal injury. RFT was used to incubate the lipopolysaccharide (LPS)-treated IEC-6 cells for determining the role of RFT in sepsis-induced intestinal injury and the underlying mechanism. The determination of cell viability and inflammation of LPS-treated IEC-6 cells influenced by RFT was conducted by Cell counting Kit-8 (CCK-8), RT-qPCR, and western blot, while the detection of LDH, diamine oxidase (DAO), and intestinal-type fatty acid binding proteins (I-FABP) was conducted for determining the intestinal cytotoxicity in these cells. The apoptosis of these cells was detected by TUNEL, with autophagy-related protein expression measured by western blot to confirm whether autophagy was activated. Finally, the aforementioned assays were conducted again after 3-Methyladenine (3-MA), an autophagy inhibitor, was used on these cells to investigate whether RFT exerted its effects on LPS-treated IEC-6 cells via modulation of autophagy. RFT alleviates LPS-induced IEC-6 cell inflammation, cytotoxicity and apoptosis, and autophagy-related proteins were expressed at higher levels when RFT was used on these cells. Nevertheless, further treatment of 3-MA weakened the restorative impacts of RFT on the inflammation, cytotoxicity and apoptosis of these cells. To conclude, this paper is the first to present evidence that RFT attenuates sepsis-induced intestinal injury by inducing autophagy, which will provide instructions for the future investigations into the use of RFT in treatment of intestinal injury.
format article
author Mingli Wang
Shiqi Guo
Yu Zhang
Yao Zhang
Hong Zhang
author_facet Mingli Wang
Shiqi Guo
Yu Zhang
Yao Zhang
Hong Zhang
author_sort Mingli Wang
title Remifentanil attenuates sepsis-induced intestinal injury by inducing autophagy
title_short Remifentanil attenuates sepsis-induced intestinal injury by inducing autophagy
title_full Remifentanil attenuates sepsis-induced intestinal injury by inducing autophagy
title_fullStr Remifentanil attenuates sepsis-induced intestinal injury by inducing autophagy
title_full_unstemmed Remifentanil attenuates sepsis-induced intestinal injury by inducing autophagy
title_sort remifentanil attenuates sepsis-induced intestinal injury by inducing autophagy
publisher Taylor & Francis Group
publishDate 2021
url https://doaj.org/article/8fc418efd67941af9e0519f3610caac2
work_keys_str_mv AT mingliwang remifentanilattenuatessepsisinducedintestinalinjurybyinducingautophagy
AT shiqiguo remifentanilattenuatessepsisinducedintestinalinjurybyinducingautophagy
AT yuzhang remifentanilattenuatessepsisinducedintestinalinjurybyinducingautophagy
AT yaozhang remifentanilattenuatessepsisinducedintestinalinjurybyinducingautophagy
AT hongzhang remifentanilattenuatessepsisinducedintestinalinjurybyinducingautophagy
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