Effect of dexmedetomidine on acute lung injury in experimental ischemia–reperfusion model

Küçükebe, Ömer Burak; Özzeybek, Deni̇z; Abdullayev, Ruslan; Ustaoğlu, Adil; Tekmen, Işıl; Küme, Tuncay

doi:10.1016/j.bjane.2015.08.002

Cited by 12 publications

(9 citation statements)

References 27 publications

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“…The animal models were referred to previously published article . The animals were randomly divided into four groups of seven animals each (n = 7).…”

Section: Methodsmentioning

confidence: 99%

“…Dexmedetomidine (DEX) is a selective α2‐adrenergic agonist widely used as a sedative in clinical anesthesia, intensive care unit management, and pain treatment . Recent in vitro and in vivo studies indicated that DEX has anti‐inflammatory activity and exerts potential protective effects against I/R‐induced skeletal muscle injury, and even remote organs like the lungs . DEX may lower the level of proinflammatory mediators IL‐1β and TNF‐α by stimulating α‐adrenoceptors .…”

Section: Introductionmentioning

confidence: 99%

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Dexmedetomidine protects against lung injury induced by limb ischemia‐reperfusion via the TLR4/MyD88/NF‐κB pathway

Xue

Chen

Tang

et al. 2019

The Kaohsiung J of Med Scie

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Dexmedetomidine (DEX) can protect the lung from ischemia-reperfusion (I/R) injury, but the underlying mechanisms are not fully understood. The aims of this study were to determine whether DEX attenuates lung injury following lower extremity I/R and to investigate the related toll-like receptor 4 (TLR4) signaling pathway. Twenty-eight SD rats were divided into four groups (n = 7): Sham, I/R, I/R + DEX (25 μg/kg prior to ischemia), and I/R + DEX + Atip (250 μg/kg atipamezole before DEX treatment). Lower extremity I/R was induced by left femoral artery clamping for 3 hours and followed by 2 hours reperfusion. Quantitative alveolar damage and the wet/dry (W/D) ratio were calculated. Interleukin (IL)-1, IL-6, and tumor necrosis factor (TNF)α in the bronchoalveolar lavage fluid (BALF) and serum and myeloperoxidase (MPO) in the lung were measured. The TLR4 and MyD88 mRNA expression levels were measured by RT-PCR, nuclear factor (NF)-κB, and phosphorylated NF-κB by western blot, respectively. Quantitative alveolar damage, W/D ratio, MPO, BALF and serum IL-1, IL-6, and TNF-α, and TLR4, MyD88, NF-κB, and p-NF-κB expression significantly increased in the I/R group relative to the Sham group. DEX preconditioning significantly reduced lung edema, and histological injury relative to the I/R group. Serum and BALF IL-1, IL-6, and TNF-α levels, MPO activity and TLR4, MyD88, NF-κB, and p-NF-κB expression were also significantly reduced in the I/R + DEX group compared with the I/R group. Atipamezole partially reversed all the aforementioned effects. DEX preconditioning protects the lungs against lower extremity I/R injury via α2-adrenoceptor-dependent and α2-adrenoceptor-independent mechanisms. It also suppresses the TLR4 pathway and reduces inflammation. K E Y W O R D S acute lung injury, dexmedetomidine, limb ischemia/reperfusion injury, toll-like receptor 4

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“…The animal models were referred to previously published article . The animals were randomly divided into four groups of seven animals each (n = 7).…”

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Dexmedetomidine protects against lung injury induced by limb ischemia‐reperfusion via the TLR4/MyD88/NF‐κB pathway

Xue

Chen

Tang

et al. 2019

The Kaohsiung J of Med Scie

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“…In clinics, Dex is used as an anxiety reducing, sedative, and pain medication. Recently, several studies have reported that Dex could be used to attenuate acute lung injury in animal models …”

Section: Discussionmentioning

confidence: 99%

Dexmedetomidine attenuates lipopolysaccharide induced acute lung injury by targeting NLRP3 via miR‐381

Zhang

Wang

Liu

et al. 2018

J Biochem & Molecular Tox

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Dexmedetomidine (Dex) is an agonist of α2-adrenergic receptors, and it is used as an anxiety reducing, sedative, and pain medication in clinical. Studies have shown that dexmedetomidine protects against lipopolysaccharide (LPS)-induced acute lung injury; however, the underlying mechanism is still unclear. To investigate, an acute lung injury mouse model was induced by intraperitoneal injection of LPS. Histopathological changes were determined by hematoxylin and eosin staining. Enzyme-linked immunosorbent assay was used to detect cytokines in serum. microRNA expression levels were detected by quantitative reverse transcription polymerase chain reaction. Protein levels were detected by western blot. Dex treatment significantly attenuated lung injury and inhibited the expression levels of the inflammation factors via reducing the level of NACHT, LRR, and PYD domains-containing protein 3 (NLRP3) and autocleavage of caspase-1. Moreover, mmu-miR-381, which targets the mRNA of NLRP3, was upregulated after Dex treatment. Dex attenuates LPS-induced acute lung injury via miR-381-targeted NLRP3.

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“…Previous studies reported that I/R injury caused disturbance of cellular homeostasis in lung, and pulmonary microvascular permeability was increased following limb ischemia [6]. Reperfusion of the acute ischemic tissue triggers a potent production of reactive oxygen species (ROS) and cytokines, which promotes a proin ammatory state and subsequently increases lung vulnerability to further injury [1,4,7,8]. Although several treatment strategies have been proposed to attenuate the remote organ injury following tourniquet use, most of them were limited to animal experiments and no ideal treatment was proved to improve prognosis [9,10].…”

Section: Introductionmentioning

confidence: 99%

Transcutaneous Electrical Acupoint Stimulation Attenuates Lung Injury Caused by Tourniquet-induced Limb Ischemia/reperfusion During Lower Extremity Surgery: A Randomized Controlled Trial

Gong

Zhao

et al. 2020

Preprint

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Background: Tourniquet-induced extremity ischemia-reperfusion injury is one of the major complications in patients with lower extremity surgery, while lung is the most vulnerable organ to insult subsequent to ischemia-reperfusion. Current scientific research data has shown that electric stimulation at special acupoints could suppress inflammasome activation and subsequently exert protective effects in the lungs. Thus, the effect of transcutaneous electrical acupuncture point stimulation (TEAS) on lung injury induced by limb ischemia/reperfusion remains to be elucidated. Methods: One hundred individuals scheduled for unilateral lower extremity surgery were randomly divided into 2 groups (n=50 each): transcutaneous electrical acupoint stimulation group (group T) and control group (group C). Patients in group T were given TEAS at FeiShu (BL13, bilateral) acupoints and ZuSanLi (ST36, non-surgical side) acupoint, while patients in group C received sham stimulation (no current) at the same acupoints for the same time as the TEAS group. Arterial blood samples were collected to assess blood gas analysis and other indicators. Results: The TEAS group showed significant improvements in blood gas analysis. Compared with group C, PaO2 and oxygenation index (OI) in group T were significantly increased at T4(4h after removing the tourniquet), while A-aDO2 and respiratory index (RI) were decreased at T4. There was an increase in the HO-1 levels in group T at T3(2h after removing the tourniquet) and T4 compared with group C. Compared with group T, SOD levels were signiﬁcantly lower at T4 in group C. At T4, the levels of ICAM-1, IL-6 and IL8 were significantly lower in group T when compared to group C. At T3 and T4, IL-10 levels were higher when compared to group C, while TNF-a levels were significantly lower.Conclusions: Transcutaneous electrical acupoint stimulation attenuates lung injury following tourniquet-induced extremity ischemia-reperfusion in patients, and HO-1 is endowed of potential mechanism of cytoprotective effects against tourniquet-induced lung injury. Trial registration: Chinese Clinical Trial Registry, ChiCTR-IOR-16008264. Registered 11 April 2016, http://www.chictr.org.cn/ ChiCTR-IOR-16008264

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Effect of dexmedetomidine on acute lung injury in experimental ischemia–reperfusion model

Abstract: Dexmedetomidine is effective in reduction of the experimental ischemia-reperfusion induced pulmonary tissue injury in rats, formed by extremity tourniquet application.

Cited by 12 publications

References 27 publications

Dexmedetomidine protects against lung injury induced by limb ischemia‐reperfusion via the TLR4/MyD88/NF‐κB pathway

Dexmedetomidine protects against lung injury induced by limb ischemia‐reperfusion via the TLR4/MyD88/NF‐κB pathway

Dexmedetomidine attenuates lipopolysaccharide induced acute lung injury by targeting NLRP3 via miR‐381

Transcutaneous Electrical Acupoint Stimulation Attenuates Lung Injury Caused by Tourniquet-induced Limb Ischemia/reperfusion During Lower Extremity Surgery: A Randomized Controlled Trial

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