Lipoxin A4 attenuates LPS-induced mouse acute lung injury via Nrf2-mediated E-cadherin expression in airway epithelial cells

Cheng, Xue; He, Songqing; Yuan, Jing; Miao, Shuo; Gao, Hongyu; Zhang, Jingnong; Yang, Li; Peng, Wei; Wu, Ping

doi:10.1016/j.freeradbiomed.2016.01.026

Cited by 61 publications

(53 citation statements)

References 78 publications

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“…Moreover, exposure to different stimuli is known to result in the generation of ROS in airway epithelial cells (Levine, ). Excessive ROS could boost inflammatory signaling in neutrophils and promote a significant increase in their chemotactic activity via a paracrine mechanism, which would further induce apoptosis in the upper respiratory compartment (Cheng et al, ; Neff et al, ). Therefore, inhibition of ROS generation should be effective against LPS‐induced ALI (Chen et al, ).…”

Section: Discussionmentioning

confidence: 99%

“…Lv et al ()showed that Nrf2‐deficient mice are more susceptible to lung damage and that Nrf2 activation suppresses LPS‐induced nucleotide‐binding domain‐like receptor protein 3 inflammasomes and the nuclear factor‐κB (NF‐κB) signaling pathway. The results from another research group demonstrated that activating the Nrf2 pathway by Nrf2 Ser40 phosphorylation and nuclear translocation leads to recovery of E‐cadherin expression, reducing airway permeability and protecting mice from LPS‐induced inflammation in airway epithelial cells (Cheng et al, ). In our current investigation, berberine administration alone dose dependently increased Nrf2 expression and nuclear accumulation in LPS‐induced 16HBE cells or ALI mice.…”

Section: Discussionmentioning

confidence: 99%

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Berberine ameliorates lipopolysaccharide‐induced acute lung injury via the PERK‐mediated Nrf2/HO‐1 signaling axis

Liang

Fan

Yan

et al. 2018

Phytotherapy Research

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A fundamental element of acute lung injury (ALI) is the inflammatory response, which can affect the entire respiratory system, including the respiratory tract and alveoli.Berberine has gained attention because of its anti-inflammatory effects. Nuclear factor-erythroid 2-related factor 2 (Nrf2) and endoplasmic reticulum (ER) stress are involved in lung injury. Nrf2 also acts as a protein kinase-like ER kinase (PERK) substrate in heart disease. Therefore, this study investigated the effect of berberine against lipopolysaccharide (LPS)-induced ALI and the role of the PERK-mediated Nrf2/HO-1 signaling axis. Berberine promoted Nrf2 nuclear translocation and phosphorylation in vitro. After LPS stimulation, this effect was further enhanced, whereas inflammatory factor (IL-6 and IL-8) release and reactive oxygen species generation were significantly decreased. Berberine effectively alleviated lung injury by reducing lung edema and neutrophil infiltration. Berberine also significantly reduced histopathological inflammatory changes via inhibition of ER stress and activation of Nrf2 signaling. Thapsigargin-induced ER stress and small interference RNA (siRNA)-mediated Nrf2 inhibition abrogated the protective effects of berberine in vitro, whereas siRNA-mediated suppression of ER stress and sulforaphane-induced Nrf2 activation further improved those effects. Importantly, ER stress induction led to Nrf2 activation, whereas PERK depletion partly reduced the level of Nrf2 phosphorylation and translocation in LPS-induced cells. Therefore, berberine inhibits LPS-induced ALI through the PERK-mediated Nrf2/HO-1 signaling axis.KEYWORDS acute lung injury (ALI), berberine, lipopolysaccharide (LPS), nuclear factor-erythroid 2-related factor 2 (Nrf2), protein kinase-like ER kinase (PERK)

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Berberine ameliorates lipopolysaccharide‐induced acute lung injury via the PERK‐mediated Nrf2/HO‐1 signaling axis

Liang

Fan

Yan

et al. 2018

Phytotherapy Research

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“…(A) RvD1 analog down-regulates the migration of PMNs isolated from human peripheral blood, by decreasing actin polymerization, and blocking LTB4-regulated adhesion molecules, 2 integrins. ( Krishnamoorthy et al, 2010 ); (B) LXA4 down-regulates VCAM-1 receptor and PMN adhesion to human endothelial cells ( Codagnone et al, 2017 ); (C) AT-LXA4 (15-epi-LXA4) down-regulates IL-8 synthesis and secretion, in human PMNs isolated from venous blood ( Jozsef et al, 2002 ); (D) RvD1 down-regulates toll-like receptor (TLR), cytokines synthesis and enhances phagocytosis of murine lung macrophage ( Codagnone et al, 2018 ); and enhances phagocytosis and bacterial killing in human CF alveolar macrophage ( Ringholz et al, 2018 ); (E) RvD1 stimulates murine macrophage differentiation from M1 to M2 state ( Recchiuti et al, 2014 ); (F) RvD1 stimulates efferocytosis of apoptotic PMNs, through the regulation of NF-κB pathways, in murine macrophage ( Lee et al, 2013 ); (G) RvD1 inhibits ROS production and increases murine macrophage survival after efferocytosis ( Lee and Surh, 2013 ); (H) RvD1 inhibits cytokines secretion by preventing IκB degradation in CF human airway epithelial cell ( Ringholz et al, 2018 ); (I) LXA4 inhibits oxidative stress and protects E-cadherin, in human airway epithelial cell ( Cheng et al, 2016 ); (J) RvD1, RvD2, and Mar1 regulate the adaptive response, enhance the differentiation to T reg rather than T H 1 and T H 17, in human peripheral blood lymphocytes ( Chiurchiù et al, 2016 ).…”

Section: Impact Of Spm S Demonstrated In Cf Modelsmentioning

confidence: 99%

The Role of Specialized Pro-Resolving Mediators in Cystic Fibrosis Airways Disease

2020

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Cystic Fibrosis (CF) is a recessive genetic disease due to mutations of the Cystic Fibrosis Transmembrane Conductance Regulator ( CFTR ) gene encoding the CFTR chloride channel. The ion transport abnormalities related to CFTR mutation generate a dehydrated airway surface liquid (ASL) layer, which is responsible for an altered mucociliary clearance, favors infections and persistent inflammation that lead to progressive lung destruction and respiratory failure. The inflammatory response is normally followed by an active resolution phase to return to tissue homeostasis, which involves specialized pro-resolving mediators (SPMs). SPMs promote resolution of inflammation, clearance of microbes, tissue regeneration and reduce pain, but do not evoke unwanted immunosuppression. The airways of CF patients showed a decreased production of SPMs even in the absence of pathogens. SPMs levels in the airway correlated with CF patients’ lung function. The prognosis for CF has greatly improved but there remains a critical need for more effective treatments that prevent excessive inflammation, lung damage, and declining pulmonary function for all CF patients. This review aims to highlight the recent understanding of CF airway inflammation and the possible impact of SPMs on functions that are altered in CF airways.

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“…LA4 has been used to remedy bronchopulmonary dysplasia, psoriasis, subarachnoid haemorrhage, and testis injury after testicular torsion/detorsion . LA4 also possesses potent anti‐inflammatory activity in response to lung injury . Recently‐reported data have shown that LA4 has therapeutic benefits in sepsis‐associated hepatic dysfunction and myocardial ischaemia–reperfusion injury …”

Section: Introductionmentioning

confidence: 99%

Lipoxin A4 ameliorates renal ischaemia–reperfusion‐induced acute lung injury in rats

Liu

Qian

Chang

2018

Clin Exp Pharma Physio

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Lipoxin A4 (LA4), a bioactive product of arachidonic acid, has been shown to exert strong anti-inflammatory activity. By contrast, the anti-inflammatory action of LA4 in a renal ischaemia-reperfusion (RIR)-mediated acute lung inflammation (ALI) model and the potential pathogenesis of the condition is still unclear. The aim of the current research was to investigate the effect of LA4 on RIR-induced ALI. The rat ALI model was induced by RIR. LA4 was injected via the tail vein immediately after RIR. The results indicate that LA4 markedly inhibits inflammatory cells infiltration, attenuates myeloperoxidase activity, and reduces the concentration of inflammatory mediators and Toll-like receptor 4 (TLR4) in RIR-induced ALI. Furthermore, LA4 suppressed nuclear factor kappa B (NF-κB) p65 and mitogen-activated protein kinase (MAPK) activation. The protective effect of LA4 in RIR-stimulated ALI was reversed by BOC-2 (an antagonist of the LA4 receptor). These results indicate that LA4 exerts powerful anti-inflammatory functions in RIR-induced ALI by attenuating TLR4 expression via MAPK and NF-κB signalling. Accordingly, LA4 might be an underlying treatment drug for RIR-induced ALI.

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Lipoxin A4 attenuates LPS-induced mouse acute lung injury via Nrf2-mediated E-cadherin expression in airway epithelial cells

Cited by 61 publications

References 78 publications

Berberine ameliorates lipopolysaccharide‐induced acute lung injury via the PERK‐mediated Nrf2/HO‐1 signaling axis

Berberine ameliorates lipopolysaccharide‐induced acute lung injury via the PERK‐mediated Nrf2/HO‐1 signaling axis

The Role of Specialized Pro-Resolving Mediators in Cystic Fibrosis Airways Disease

Lipoxin A4 ameliorates renal ischaemia–reperfusion‐induced acute lung injury in rats

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