Usnic acid protects LPS-induced acute lung injury in mice through attenuating inflammatory responses and oxidative stress

Su, Zuowei; Mo, Zhi-Zhun; Liao, Jin-Bin; Feng, Xue-Xuan; Liang, Yingmin; Xie, Zhaoxiong; Liu, Yuhong; Chen, Xiaoying; Chen, Zhiwei; Su, Zi‐Ren; Lai, Xiaoping

doi:10.1016/j.intimp.2014.06.043

Cited by 98 publications

(48 citation statements)

References 30 publications

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“…Studies have shown that neutrophil migration into the lung is at least partially mediated by the chemokines MIP-2 and KC (Lomas-Neira et al 2004). Indeed, both MIP-2 and KC have been linked to acute lung injury caused by systemic LPS (Wang et al 2013; Su et al 2014) by mediating neutrophil recruitment via activation of CXCR2 (Reutershan et al 2006). The work presented here shows that LPS-induced MIP-2 and KC expression in the lung was enhanced by ethanol exposure.…”

Section: Discussionmentioning

confidence: 99%

Chronic Alcohol Exposure Enhances Lipopolysaccharide-Induced Lung Injury in Mice: Potential Role of Systemic Tumor Necrosis Factor-Alpha

Massey

Poole

Siow

et al. 2015

Alcohol Clin Exp Res

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Background It is well known that liver and lung injury can occur simultaneously during severe inflammation (e.g. multiple organ failure). However, whether these are parallel or interdependent (i.e. liver:lung axis) mechanisms is unclear. Previous studies have shown that chronic ethanol consumption greatly increases mortality in the setting of sepsis-induced acute lung injury (ALI). The potential contribution of subclinical liver disease in driving this effect of Ethanol on the lung remains unknown. Therefore, the purpose of this study was to characterize the impact of chronic Ethanol exposure on concomitant liver and lung injury. Methods Male mice were exposed to ethanol-containing Lieber-DeCarli diet or pair-fed control diet for 6 weeks. Some animals were administered lipopolysaccharide (LPS) 4 or 24 hours prior to sacrifice to mimic sepsis-induced ALI. Some animals received the TNFα blocking drug, etanercept, for the duration of alcohol exposure. The expression of cytokine mRNA in lung and liver tissue was determined by qPCR. Cytokine levels in the bronchoalveolar lavage fluid (BALF) and plasma were determined by Luminex assay. Results As expected, the combination of Ethanol and LPS caused liver injury, as indicated by significantly increased levels of the transaminases ALT/AST in the plasma and by changes in liver histology. In the lung, Ethanol preexposure enhanced pulmonary inflammation and alveolar hemorrhage caused by LPS. These changes corresponded with unique alterations in the expression of pro-inflammatory cytokines in the liver (i.e TNFα) and lung (i.e. MIP-2, KC). Systemic depletion of TNFα (etanercept) blunted injury and the increase in MIP-2 and KC caused by the combination of ethanol and LPS in the lung. Conclusions Chronic Ethanol preexposure enhanced both liver and lung injury caused by LPS. Enhanced organ injury corresponded with unique changes in the pro-inflammatory cytokine expression profiles in the liver and the lung.

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Section: Discussionmentioning

confidence: 99%

Chronic Alcohol Exposure Enhances Lipopolysaccharide-Induced Lung Injury in Mice: Potential Role of Systemic Tumor Necrosis Factor-Alpha

Massey

Poole

Siow

et al. 2015

Alcohol Clin Exp Res

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“…At the highest dose, it worked comparably with ibuprofen (100 mg/kg) and the paw edema measured in ml was 0.55 for the tested substance and 0.47 for the reference substance [17]. The next study where usnic acid was tested as an anti-infammatory factor was conducted by Su et al [18]. Authors noted that usnic acid attenuated inflammatory responses of acute lung injury in mice induced by lipopolysaccharide.…”

Section: Usnic Acidmentioning

confidence: 99%

“…Authors noted that usnic acid attenuated inflammatory responses of acute lung injury in mice induced by lipopolysaccharide. It was proven that usnic acid lowered the expression of pro-inflammatory cytokines including tumor necrosis factor alpha (TNF-α), interleukin-6 (IL-6) but also anti-inflammatory interleukin-8 (IL-8) and macrophage inflammatory protein-2 (MIP-2) and improved level of anti-inflammatory cytokine in the bronchoalveolar lavage fluid [18].…”

Section: Usnic Acidmentioning

confidence: 99%

Lichens as a source of chemical compounds with anti-inflammatory activity

Studzińska-Sroka

Dubino

2018

Herba Polonica

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SummarySymptoms of inflammation accompany a number of diseases. In order to mitigate them, folk medicine has used a variety of medicinal substances, including herbs and mushrooms. Lichens are less known organisms, containing specific secondary metabolites with interesting biological properties. One of their biological actions is the anti-inflammatory activity that has been confirmed by in vitro and animal studies. It has been proven that compounds and extracts from lichens inhibit the enzymes involved in the inflammatory process. The following paper is a review of research on the little-known anti-inflammatory properties of lichens.

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“…Other compounds with remarkably good anti-oxidative and anti-inflammatory effects have been studied for the purpose of reducing the inflammatory effects of the oxidative stress on pulmonary tissue, among which pentoxifylline [115], apocynin-nitrone [116], narginin [117], sphingisylphosphorylcholine [118], usnic acid [119], zinc aspartate [120], trapidil [121] or melatonin [122].…”

Section: Therapy With Antioxidantsmentioning

confidence: 99%

Oxidative stress in severe pulmonary trauma in critical ill patients. Antioxidant therapy in patients with multiple trauma — a review

Bedreag¹,

Rogobete

Sărăndan³

et al. 2015

Anaesthesiol Intensive Ther

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Multiple trauma patients require extremely good management and thus, the trauma team needs to be prepared and to be up to date with the new standards of intensive therapy. Oxidative stress and free radicals represent an extremely aggressive factor to cells, having a direct consequence upon the severity of lung inflammation. Pulmonary tissue is damaged by oxidative stress, leading to biosynthesis of mediators that exacerbate inflammation modulators. The subsequent inflammation spreads throughout the body, leading most of the time to multiple organ dysfunction and death. In this paper, we briefly present an update of biochemical effects of oxidative stress and free radical damage to the pulmonary tissue in patients in critical condition in the intensive care unit. Also, we would like to present a series of active substances that substantially reduce the aggressiveness of free radicals, increasing the chances of survival.

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Usnic acid protects LPS-induced acute lung injury in mice through attenuating inflammatory responses and oxidative stress

Cited by 98 publications

References 30 publications

Chronic Alcohol Exposure Enhances Lipopolysaccharide-Induced Lung Injury in Mice: Potential Role of Systemic Tumor Necrosis Factor-Alpha

Chronic Alcohol Exposure Enhances Lipopolysaccharide-Induced Lung Injury in Mice: Potential Role of Systemic Tumor Necrosis Factor-Alpha

Lichens as a source of chemical compounds with anti-inflammatory activity

Oxidative stress in severe pulmonary trauma in critical ill patients. Antioxidant therapy in patients with multiple trauma — a review

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