Electroacupuncture Alleviate Lung Injury of Sepsis Through α7nAChR and NF-κB Signaling Pathway

Abstract Background Sepsis is the leading cause of death in hospitalized patients in the intensive care unit (ICU). Although substantial progress has been made in studies on the treatment of sepsis, the mortality rate remains extremely high. We have previously reported that electroacupuncture (EA) i...

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Main Authors: Xingxing Shi, Lixia Du, Zhongmin Fan, Binxiao Su, Yu Chen, Zongping Fang, Xijing Zhang
Format: Article
Language:English
Published: Springer 2022-07-01
Series:Intensive Care Research
Subjects:
Online Access:https://doi.org/10.1007/s44231-022-00008-1
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author Xingxing Shi
Lixia Du
Zhongmin Fan
Binxiao Su
Yu Chen
Zongping Fang
Xijing Zhang
author_facet Xingxing Shi
Lixia Du
Zhongmin Fan
Binxiao Su
Yu Chen
Zongping Fang
Xijing Zhang
author_sort Xingxing Shi
collection DOAJ
description Abstract Background Sepsis is the leading cause of death in hospitalized patients in the intensive care unit (ICU). Although substantial progress has been made in studies on the treatment of sepsis, the mortality rate remains extremely high. We have previously reported that electroacupuncture (EA) induced tolerance against sepsis, but the underlying mechanism remains unclear. Methods C57BL/6 mice were pretreated with EA before sepsis was induced by cecal ligation and puncture (CLP). Then the indexes associated with pulmonary edema and mortality were tested. And the changes of endogenous cholinergic anti-inflammatory pathway especially their typical receptor α7nAChR were detected. Finally, the mechanism of EA in sepsis was explored through regulating the expression of α7nAChR. Results The expression of α7nAChR was significantly decreased after sepsis, while EA prevented this reduction. Methyllycaconitine (MLA), an antagonist of α7nAChR, attenuated the beneficial effects of EA. On the other hand, as an α7nAChR agonist, GTS-21 produced similar protective effects against sepsis. Furthermore, the EA-induced enhancement of α7nAChR and inhibition of NF-κB expression in the lungs were reversed by MLA administration. Conclusions EA robustly protects the lungs against sepsis and inhibits NF-κB release by activating α7nAChR in mice.
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spelling doaj.art-6602d2a72e3847a8954caa1afd9a0b9f2023-11-05T12:19:11ZengSpringerIntensive Care Research2666-98622022-07-0121-2344310.1007/s44231-022-00008-1Electroacupuncture Alleviate Lung Injury of Sepsis Through α7nAChR and NF-κB Signaling PathwayXingxing Shi0Lixia Du1Zhongmin Fan2Binxiao Su3Yu Chen4Zongping Fang5Xijing Zhang6Department of Critical Care Medicine and Department of Anesthesiology Perioperative Medicine, Xijing Hospital, Fourth Military Medical UniversityDepartment of Critical Care Medicine and Department of Anesthesiology Perioperative Medicine, Xijing Hospital, Fourth Military Medical UniversityDepartment of Critical Care Medicine and Department of Anesthesiology Perioperative Medicine, Xijing Hospital, Fourth Military Medical UniversityDepartment of Critical Care Medicine and Department of Anesthesiology Perioperative Medicine, Xijing Hospital, Fourth Military Medical UniversityDepartment of Critical Care Medicine and Department of Anesthesiology Perioperative Medicine, Xijing Hospital, Fourth Military Medical UniversityDepartment of Critical Care Medicine and Department of Anesthesiology Perioperative Medicine, Xijing Hospital, Fourth Military Medical UniversityDepartment of Critical Care Medicine and Department of Anesthesiology Perioperative Medicine, Xijing Hospital, Fourth Military Medical UniversityAbstract Background Sepsis is the leading cause of death in hospitalized patients in the intensive care unit (ICU). Although substantial progress has been made in studies on the treatment of sepsis, the mortality rate remains extremely high. We have previously reported that electroacupuncture (EA) induced tolerance against sepsis, but the underlying mechanism remains unclear. Methods C57BL/6 mice were pretreated with EA before sepsis was induced by cecal ligation and puncture (CLP). Then the indexes associated with pulmonary edema and mortality were tested. And the changes of endogenous cholinergic anti-inflammatory pathway especially their typical receptor α7nAChR were detected. Finally, the mechanism of EA in sepsis was explored through regulating the expression of α7nAChR. Results The expression of α7nAChR was significantly decreased after sepsis, while EA prevented this reduction. Methyllycaconitine (MLA), an antagonist of α7nAChR, attenuated the beneficial effects of EA. On the other hand, as an α7nAChR agonist, GTS-21 produced similar protective effects against sepsis. Furthermore, the EA-induced enhancement of α7nAChR and inhibition of NF-κB expression in the lungs were reversed by MLA administration. Conclusions EA robustly protects the lungs against sepsis and inhibits NF-κB release by activating α7nAChR in mice.https://doi.org/10.1007/s44231-022-00008-1SepsisElectroacupunctureCholinergic anti-inflammatory pathwayα7 nicotinic acetylcholine receptorNF-κB
spellingShingle Xingxing Shi
Lixia Du
Zhongmin Fan
Binxiao Su
Yu Chen
Zongping Fang
Xijing Zhang
Electroacupuncture Alleviate Lung Injury of Sepsis Through α7nAChR and NF-κB Signaling Pathway
Intensive Care Research
Sepsis
Electroacupuncture
Cholinergic anti-inflammatory pathway
α7 nicotinic acetylcholine receptor
NF-κB
title Electroacupuncture Alleviate Lung Injury of Sepsis Through α7nAChR and NF-κB Signaling Pathway
title_full Electroacupuncture Alleviate Lung Injury of Sepsis Through α7nAChR and NF-κB Signaling Pathway
title_fullStr Electroacupuncture Alleviate Lung Injury of Sepsis Through α7nAChR and NF-κB Signaling Pathway
title_full_unstemmed Electroacupuncture Alleviate Lung Injury of Sepsis Through α7nAChR and NF-κB Signaling Pathway
title_short Electroacupuncture Alleviate Lung Injury of Sepsis Through α7nAChR and NF-κB Signaling Pathway
title_sort electroacupuncture alleviate lung injury of sepsis through α7nachr and nf κb signaling pathway
topic Sepsis
Electroacupuncture
Cholinergic anti-inflammatory pathway
α7 nicotinic acetylcholine receptor
NF-κB
url https://doi.org/10.1007/s44231-022-00008-1
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