Role and Mechanism of Maresin-1 in Acute Lung Injury Induced by Trauma-Hemorrhagic Shock

Ma, Huayi; Mo, Song; Yi, Qushen; Junhua, Lai; Liu, Huan; Shi, Zhanying

doi:10.12659/msm.923518

Cited by 8 publications

(7 citation statements)

References 28 publications

(34 reference statements)

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“…The role of iNOS in liver fibrosis has been studied using iNOS knockout mice and specific iNOS inhibitors, resulting in reduced liver fibrosis [ 48 ]. Some studies have demonstrated that MaR1 suppresses iNOS levels [ 13 , 49 , 50 ]; however, here we show for first time that MaR1 suppresses iNOS in a chronic model of liver disease. MaR1 promotes an anti-inflammatory response by an enhancement of IL-10 with a concomitant decrease in proinflammatory cytokines, TNF-α and IL-1β.…”

Section: Discussioncontrasting

confidence: 50%

Maresin-1 Prevents Liver Fibrosis by Targeting Nrf2 and NF-κB, Reducing Oxidative Stress and Inflammation

Rodríguez

Sabaj

Tolosa

et al. 2021

Cells

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Liver fibrosis is a complex process characterized by the excessive accumulation of extracellular matrix (ECM) and an alteration in liver architecture, as a result of most types of chronic liver diseases such as cirrhosis, hepatocellular carcinoma (HCC) and liver failure. Maresin-1 (MaR1) is derivative of ω-3 docosahexaenoic acid (DHA), which has been shown to have pro-resolutive and anti-inflammatory effects. We tested the hypothesis that the application of MaR1 could prevent the development of fibrosis in an animal model of chronic hepatic damage. Sprague-Dawley rats were induced with liver fibrosis by injections of diethylnitrosamine (DEN) and treated with or without MaR1 for four weeks. In the MaR1-treated animals, levels of AST and ALT were normalized in comparison with DEN alone, the hepatic architecture was improved, and inflammation and necrotic areas were reduced. Cell proliferation, assessed by the mitotic activity index and the expression of Ki-67, was increased in the MaR1-treated group. MaR1 attenuated liver fibrosis and oxidative stress was induced by DEN. Plasma levels of the pro-inflammatory mediators TNF-α and IL-1β were reduced in MaR1-treated animals, whereas the levels of IL-10, an anti-inflammatory cytokine, increased. Interestingly, MaR1 inhibited the translocation of the p65 subunit of NF-κB, while increasing the activation of Nrf2, a key regulator of the antioxidant response. Finally, MaR1 treatment reduced the levels of the pro-fibrotic mediator TGF-β and its receptor, while normalizing the hepatic levels of IGF-1, a proliferative agent. Taken together, these results suggest that MaR1 improves the parameters of DEN-induced liver fibrosis, activating hepatocyte proliferation and decreasing oxidative stress and inflammation. These results open the possibility of MaR1 as a potential therapeutic agent in fibrosis and other liver pathologies.

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Section: Discussioncontrasting

confidence: 50%

Maresin-1 Prevents Liver Fibrosis by Targeting Nrf2 and NF-κB, Reducing Oxidative Stress and Inflammation

Rodríguez

Sabaj

Tolosa

et al. 2021

Cells

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“…[62][63][64][65] In this regard, SPMs, such as MaR1, exhibit important anti-inflammatory, antioxidant and cytoprotective actions in the lungs through the inhibition of NF-κB and the activation of Nrf2. 64,[66][67][68] More details about the anti-inflammatory effects on airway/respiratory disease generated by the n-3 PUFAs and their SPMs will be explained in the following paragraphs.…”

Section: Reviewmentioning

confidence: 99%

“…100 Moreover, it has been described that MaR1 promotes the resolution of acute lung injury through the accelera- tion of caspase-dependent neutrophil apoptosis by inhibiting the regulators of apoptosis (AKT, ERK, p38, BCL-2, and MCL-1). 101 Besides acute lung injury, MaR1 was assayed as a protective agent against lung trauma hemorrhagic shock 66 and ischemia-reperfusion, 68 showing protection of the lung tissue through the inhibition of TLR4/p38MAPK/NF-κB activation in the former and activation of the Nrf2 signaling pathway in the latter (Fig. 2).…”

Section: Food and Function Reviewmentioning

confidence: 99%

“…2). 66,68 Concerning acute lung inflammation, the use of metabolipidomics revealed that MaR1 is increased in the resolution phase of lungs exposed to allergic inflammation, promoting de novo lymphocyte T regulators by TGF-β modulation, with a consequent cytokine depletion and diminution of CD4 + TH 2 cells. 102 In relation to TGF-β and MaR1, it was demonstrated that MaR1 inhibits the pro-fibrotic actions of TGF-β1 related to proliferation, migration, and differentiation of fibroblasts in an in vitro model of lung fibrosis.…”

Section: Food and Function Reviewmentioning

confidence: 99%

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N-3 PUFAs and their specialized pro-resolving lipid mediators on airway inflammatory response: beneficial effects in the prevention and treatment of respiratory diseases

et al. 2022

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“…Nitric oxide synthase (NOS-2), a principal enzyme, can produce high-levels of sustained NO. NOS-2 is upregulated in most ALI models including P-ALI [53][54][55][56]. The inhibition of NOS-2 is considered as a potential treatment for ALI.…”

Section: Nos-2 Inhibitorsmentioning

confidence: 99%

Mechanism of Phosgene-Induced Acute Lung Injury and Treatment Strategy

Huang

Meng

et al. 2021

IJMS

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Phosgene (COCl2) was once used as a classic suffocation poison and currently plays an essential role in industrial production. Due to its high toxicity, the problem of poisoning caused by leakage during production, storage, and use cannot be ignored. Phosgene mainly acts on the lungs, causing long-lasting respiratory depression, refractory pulmonary edema, and other related lung injuries, which may cause acute respiratory distress syndrome or even death in severe cases. Due to the high mortality, poor prognosis, and frequent sequelae, targeted therapies for phosgene exposure are needed. However, there is currently no specific antidote for phosgene poisoning. This paper reviews the literature on the mechanism and treatment strategies to explore new ideas for the treatment of phosgene poisoning.

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Role and Mechanism of Maresin-1 in Acute Lung Injury Induced by Trauma-Hemorrhagic Shock

Cited by 8 publications

References 28 publications

Maresin-1 Prevents Liver Fibrosis by Targeting Nrf2 and NF-κB, Reducing Oxidative Stress and Inflammation

Maresin-1 Prevents Liver Fibrosis by Targeting Nrf2 and NF-κB, Reducing Oxidative Stress and Inflammation

N-3 PUFAs and their specialized pro-resolving lipid mediators on airway inflammatory response: beneficial effects in the prevention and treatment of respiratory diseases

Mechanism of Phosgene-Induced Acute Lung Injury and Treatment Strategy

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