Endogenous expression pattern of resolvin D1 in a rat model of self-resolution of lipopolysaccharide-induced acute respiratory distress syndrome and inflammation

Sun, Wei; Zai-ping, Wang; Gui, Ping; Xia, Weiyi; Xia, Zhengyuan; Zhang, Xing-cai; Deng, Qingzhu; Xuan, Wei; Marie, Christelle; Wang, Linlin; Wu, Qingping; Wang, Tingting; Lin, Yun

doi:10.1016/j.intimp.2014.09.001

Cited by 20 publications

(16 citation statements)

References 27 publications

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“…Therefore, our in vivo study used international studies and our previous studies to select the intravenous LPS 5 mg/kg method to model ALI/ARDS in rats20. Consistent with earlier findings, after an injection of LPS for 6 h, lung inflammatory cells were increased, and IL-6 and IL-10 levels were significantly increased; therefore, we used 6 h as the observation point for our study21. Moreover, to determine the role of HO-1 induction in LPS-induced ALI/ARDS, we also treated with ZnPP-IX, which acts as a selective competitive enzyme for HO-1 compared to other microsomal enzymes22.…”

Section: Discussionmentioning

confidence: 54%

Effect of Heme Oxygenase-1 on Mitofusin-1 protein in LPS-induced ALI/ARDS in rats

Wang

et al. 2016

Sci Rep

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Acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) is a common and important oxidative stress in the lung. Mitochondrial fusion responds to the normal morphology and function of cells and is finely regulated by mitochondrial fusion proteins, such as mitofusin-1 protein (Mfn1), mitofusin-2 protein (Mfn2) and optical atrophy 1 (OPA1). Additionally, Mfn1 has been identified as the most important protein in mitochondrial fusion. Heme oxygenase-1 (HO-1) is a stress-inducible protein that plays a critical role in protecting against oxidative stress. However, whether the protection of HO-1 is related to mitochondrial fusion is still a question. Thus, our in vitro and in vivo experiments aimed to identify the relationship between HO-1 and Mfn1. Here, we used Hemin and ZnPP-IX as treatments in an in vivo experiment. Then, HO-1 and Mfn1 were measured using RT-PCR and Western blotting. Supernatants were analyzed for MDA, SOD, and ROS. Our results implied that HO-1 upregulation suppressed oxidative stress induced by LPS, and the possible mechanism could be associated with Mfn1 and the PI3K/Akt pathway.

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Section: Discussionmentioning

confidence: 54%

Effect of Heme Oxygenase-1 on Mitofusin-1 protein in LPS-induced ALI/ARDS in rats

Wang

et al. 2016

Sci Rep

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“…Furthermore, the timing of MaR1 production appears specific and regulated, as does the production of RvD1 (REF. 137). Together, these findings highlight the potential roles SPMs could have in decreasing the severity and duration of ARDS and, more generally, the data support a targeted pro-resolving approach as a new therapeutic strategy for this devastating condition that is currently without available medical treatment.…”

Section: Spms In Chronic Inflammatory Diseasesmentioning

confidence: 99%

Specialized pro-resolving mediators: endogenous regulators of infection and inflammation

2015

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Specialized pro-resolving mediators (SPMs) are enzymatically derived from essential fatty acids and have important roles in orchestrating the resolution of tissue inflammation -that is, catabasis. Host responses to tissue infection elicit acute inflammation in an attempt to control invading pathogens. SPMs are lipid mediators that are part of a larger family of pro-resolving molecules, which includes proteins and gases, that together restrain inflammation and resolve the infection. These immunoresolvents are distinct from immunosuppressive molecules as they not only dampen inflammation but also promote host defence. Here, we focus primarily on SPMs and their roles in lung infection and inflammation to illustrate the potent actions these mediators play in restoring tissue homeostasis after an infection.Acute inflammation is a vital response to infection that is initiated within seconds of pathogen detection 1 . Granulocytes are rapidly recruited to sites of infection 2 , where they become activated and augment the resident capacity of infected tissue to kill and ultimately clear the pathogen 3 . These early events in the host response to infection are essential for survival and are coordinated by several families of pro-inflammatory mediators, including lipid mediators (such as prostaglandins and leukotrienes), cytokines and chemokines. These pro-inflammatory mediators have overlapping and distinct functions and ultimately induce an increase in vascular permeability and orchestrate leukocyte recruitment. This leads to the cardinal signs of tissue inflammation -namely calor, rubor, tumor, dolor and potentially functio laesa (FIG. 1).Recently, a new array of molecules that function in the resolution of inflammation were elucidated and named specialized pro-resolving mediators (SPMs) 4,5 . Many of these SPMs are produced during the acute inflammatory response 6 , and their structure, biosynthesis and organic synthesis have been recently reviewed (see REF. 5). Typically, acute inflammatory responses to pathogens are self-limiting, and there is a growing appreciation that SPMs have pivotal anti-inflammatory and anti-infective roles in tissue catabasis 4 . For effective Correspondence to B.D.L. blevy@partners.org. Competing interests statementThe authors declare competing interests: see Web version for details. DATABASES ClinicalTrials.gov: http://www.clinicaltrials.gov ALL LINKS ARE ACTIVE IN THE ONLINE PDF HHS Public AccessAuthor manuscript Nat Rev Immunol. Author manuscript; available in PMC 2017 January 18. Author Manuscript Author ManuscriptAuthor ManuscriptAuthor Manuscript resolution of inflammation to occur in tissues, cessation of granulocyte recruitment is required in conjunction with the recruitment and differentiation of macrophages, which help clear inflammatory cells and tissue debris to restore tissue homeostasis 7 . Granulocytes in the tissue undergo apoptosis during the resolution of inflammation to prevent bystander tissue injury occurring from the release of potentially toxic cellular conten...

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“…Acute lung injury (ALI) is characterized by the infiltration of inflammatory cells, production of inflammatory mediators and diffuse lung inflammation (Shi et al, ), leading to a high mortality rate (Sun et al, ; Ghidoni et al, ; Sharp et al, ). A variety of clinical syndromes, such as pneumonia, sepsis, major trauma, gastric content aspiration and acute pancreatitis, can induce the occurrence of ALI (Feng et al, ).…”

Section: Introductionmentioning

confidence: 99%

Mogroside IIIE Attenuates LPS‐Induced Acute Lung Injury in Mice Partly Through Regulation of the TLR4/MAPK/NF‐κB Axis via AMPK Activation

Tao

Cao

et al. 2017

Phytotherapy Research

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Acute lung injury (ALI) often leads to high mortality, and there is as yet no effective drug treatment. The present study aimed to investigate protective effects of mogroside IIIE (MGIIIE, a cucurbitane-type triterpenoid from Siraitia grosvenorii Fruits) in experimental ALI and its underlying mechanism. MGIIIE (1, 10 0r 20 mg/kg) was orally administered for 1 h before a single intratracheal administration of lipopolysaccharide (LPS, 5 mg/kg). MGIIIE treatment dose-dependently suppressed pulmonary oedema, pro-inflammatory mediators (IL-1β, IL-6, TNF-α and HMGB1) release and higher MPO activity in lung tissues induced by LPS challenge. Molecular researches showed that mogroside IIIE (20 mg/kg) not only increased the phosphorylation of adenosine 5'-monophosphate-activated protein kinase (AMPK) but suppressed the over-expression of toll-like receptor 4 (TLR4) and myeloid differentiation factor 88 (MyD88). In addition, MGIIIE also inhibited the activation of MAPKs and nuclear factor κB (NF-κB) signalling in lung tissues from LPS-challenged mice. Similar antiinflammatory effects of MGIIIE were obtained in LPS-treated macrophages. Compound C (a pharmacological AMPK inhibitor) obviously reversed the antiinflammatory effect of MGIIIE in LPS-induced ALI mice. Taken together, AMPK activation plays a crucial role in the antiinflammatory effects of MGIIIE in LPS-induced ALI by down-regulating TLR4/MAPK/NF-κB signalling pathways. Copyright © 2017 John Wiley & Sons, Ltd.

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Endogenous expression pattern of resolvin D1 in a rat model of self-resolution of lipopolysaccharide-induced acute respiratory distress syndrome and inflammation

Cited by 20 publications

References 27 publications

Effect of Heme Oxygenase-1 on Mitofusin-1 protein in LPS-induced ALI/ARDS in rats

Effect of Heme Oxygenase-1 on Mitofusin-1 protein in LPS-induced ALI/ARDS in rats

Specialized pro-resolving mediators: endogenous regulators of infection and inflammation

Mogroside IIIE Attenuates LPS‐Induced Acute Lung Injury in Mice Partly Through Regulation of the TLR4/MAPK/NF‐κB Axis via AMPK Activation

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