The protective effects of Thalictrum minus L. on lipopolysaccharide-induced acute lung injury

Abstract Background Endothelial glycocalyx loss is integral to increased pulmonary vascular permeability in sepsis-related acute lung injury. Protectin conjugates in tissue regeneration 1 (PCTR1) is a novel macrophage-derived lipid mediator exhibiting potential anti-inflammatory and pro-resolving benefits. Methods PCTR1 was administrated intraperitoneally with 100 ng/mouse after lipopolysaccharide (LPS) challenged. Survival rate and lung function were used to evaluate the protective effects of PCTR1. Lung inflammation response was observed by morphology and inflammatory cytokines level. Endothelial glycocalyx and its related key enzymes were measured by immunofluorescence, ELISA, and Western blot. Afterward, related-pathways inhibitors were used to identify the mechanism of endothelial glycocalyx response to PCTR1 in mice and human umbilical vein endothelial cells (HUVECs) after LPS administration. Results In vivo, we show that PCTR1 protects mice against lipopolysaccharide (LPS)-induced sepsis, as shown by enhanced the survival and pulmonary function, decreased the inflammatory response in lungs and peripheral levels of inflammatory cytokines such as tumor necrosis factor-α, interleukin-6, and interleukin-1β. Moreover, PCTR1 restored lung vascular glycocalyx and reduced serum heparin sulphate (HS), syndecan-1 (SDC-1), and hyaluronic acid (HA) levels. Furthermore, we found that PCTR1 downregulated heparanase (HPA) expression to inhibit glycocalyx degradation and upregulated exostosin-1 (EXT-1) protein expression to promote glycocalyx reconstitution. Besides, we observed that BAY11-7082 blocked glycocalyx loss induced by LPS in vivo and in vitro, and BOC-2 (ALX antagonist) or EX527 (SIRT1 inhibitor) abolished the restoration of HS in response to PCTR1. Conclusion PCTR1 protects endothelial glycocalyx via ALX receptor by regulating SIRT1/NF-κB pathway, suggesting PCTR1 may be a significant therapeutic target for sepsis-related acute lung injury.

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Protective effects of coumestrol on lipopolysaccharide-induced acute lung injury via the inhibition of proinflammatory mediators and NF-κB activation

Journal of Functional Foods ◽

10.1016/j.jff.2017.04.027 ◽

2017 ◽

Vol 34 ◽

pp. 181-188 ◽

Cited By ~ 6

Author(s):

Heung Joo Yuk ◽

Jae Won Lee ◽

Hyun Ah Park ◽

Ok-Kyoung Kwon ◽

Kyeong-Hwa Seo ◽

...

Keyword(s):

Acute Lung Injury ◽

Lung Injury ◽

Protective Effects ◽

Proinflammatory Mediators

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Protective effects of hydrogen gas against sepsis-induced acute lung injury via regulation of mitochondrial function and dynamics

International Immunopharmacology ◽

10.1016/j.intimp.2018.10.012 ◽

2018 ◽

Vol 65 ◽

pp. 366-372 ◽

Cited By ~ 15

Author(s):

Aili Dong ◽

Yang Yu ◽

Yanyan Wang ◽

Can Li ◽

Hongguang Chen ◽

...

Keyword(s):

Acute Lung Injury ◽

Lung Injury ◽

Mitochondrial Function ◽

Hydrogen Gas ◽

Protective Effects

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Protective effects of erythropoietin against acute lung injury in a rat model of acute necrotizing pancreatitis

World Journal of Gastroenterology ◽

10.3748/wjg.v13.i46.6172 ◽

2007 ◽

Vol 13 (46) ◽

pp. 6172 ◽

Cited By ~ 8

Author(s):

Oge Tascilar ◽

Güldeniz Karadeniz Cakmak ◽

Ishak Ozel Tekin ◽

Ali Ugur Emre ◽

Bulent Hamdi Ucan ◽

...

Keyword(s):

Acute Lung Injury ◽

Lung Injury ◽

Rat Model ◽

Necrotizing Pancreatitis ◽

Acute Necrotizing Pancreatitis ◽

Protective Effects ◽

Acute Necrotizing

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Corrigendum to “JAK2/STAT3 Pathway Was Associated with the Protective Effects of IL-22 on Aortic Dissection with Acute Lung Injury”

Disease Markers ◽

10.1155/2019/1901626 ◽

2019 ◽

Vol 2019 ◽

pp. 1-7

Author(s):

Wei Ren ◽

Zhiwei Wang ◽

Zhiyong Wu ◽

Zhipeng Hu ◽

Feifeng Dai ◽

...

Keyword(s):

Acute Lung Injury ◽

Lung Injury ◽

Aortic Dissection ◽

Protective Effects ◽

Stat3 Pathway

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Protective effects of naringin against paraquat-induced acute lung injury and pulmonary fibrosis in mice

Food and Chemical Toxicology ◽

10.1016/j.fct.2013.04.024 ◽

2013 ◽

Vol 58 ◽

pp. 133-140 ◽

Cited By ~ 66

Author(s):

Yan Chen ◽

Yi-chu Nie ◽

Yu-long Luo ◽

Feng Lin ◽

Yan-fang Zheng ◽

...

Keyword(s):

Acute Lung Injury ◽

Pulmonary Fibrosis ◽

Lung Injury ◽

Protective Effects

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Veronicastrum axillare Alleviates Lipopolysaccharide-Induced Acute Lung Injury via Suppression of Proinflammatory Mediators and Downregulation of the NF-κB Signaling Pathway

Mediators of Inflammation ◽

10.1155/2016/7934049 ◽

2016 ◽

Vol 2016 ◽

pp. 1-9 ◽

Cited By ~ 1

Author(s):

Quanxin Ma ◽

Kai Wang ◽

Qinqin Yang ◽

Shun Ping ◽

Weichun Zhao ◽

...

Keyword(s):

Acute Lung Injury ◽

Lung Injury ◽

Signaling Pathway ◽

Biological Activities ◽

Interleukin 1 ◽

Folk Medicine ◽

Protective Effects ◽

Proinflammatory Mediators ◽

Anti Inflammatory

Veronicastrum axillare is a traditional medical plant in China which is widely used in folk medicine due to its versatile biological activities, especially for its anti-inflammatory effects. However, the detailed mechanism underlying this action is not clear. Here, we studied the protective effects of V. axillare against acute lung injury (ALI), and we further explored the pharmacological mechanisms of this action. We found that pretreatment with V. axillare suppressed the release of proinflammatory cytokines in the serum of ALI mice. Histological analysis of lung tissue demonstrated that V. axillare inhibited LPS-induced lung injury, improved lung morphology, and reduced the activation of nuclear factor-κB (NF-κB) in the lungs. Furthermore, the anti-inflammatory actions of V. axillare were investigated in vitro. We observed that V. axillare suppressed the mRNA expression of interleukin-1β (IL-1β), IL-6, monocyte chemotactic protein-1 (MCP-1), cyclooxygenase-2 (COX-2), and tumor necrosis factor-α (TNF-α) in RAW264.7 cells challenged with LPS. Furthermore, pretreatment of V. axillare in vitro reduced the phosphorylation of p65 and IκB-α which is activated by LPS. In conclusion, our data firstly demonstrated that the anti-inflammatory effects of V. axillare against ALI were achieved through downregulation of the NF-κB signaling pathway, thereby reducing the production of inflammatory mediators.

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Baicalin exerts protective effects against lipopolysaccharide-induced acute lung injury by regulating the crosstalk between the CX3CL1-CX3CR1 axis and NF-κB pathway in CX3CL1-knockout mice

International Journal of Molecular Medicine ◽

10.3892/ijmm.2016.2456 ◽

2016 ◽

Vol 37 (3) ◽

pp. 703-715 ◽

Cited By ~ 23

Author(s):

XIN-MIN DING ◽

LEI PAN ◽

YONG WANG ◽

QIN-ZHI XU

Keyword(s):

Acute Lung Injury ◽

Lung Injury ◽

Knockout Mice ◽

Protective Effects

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NEMO-Binding Domain Peptide Attenuates Lipopolysaccharide-Induced Acute Lung Injury by Inhibiting the NF-κB Signaling Pathway

Mediators of Inflammation ◽

10.1155/2016/7349603 ◽

2016 ◽

Vol 2016 ◽

pp. 1-11 ◽

Cited By ~ 6

Author(s):

Jianhua Huang ◽

Li Li ◽

Weifeng Yuan ◽

Linxin Zheng ◽

Zhenhui Guo ◽

...

Keyword(s):

Acute Lung Injury ◽

Lung Injury ◽

Signaling Pathway ◽

Binding Domain ◽

Dependent Manner ◽

Protective Effects ◽

Lps Challenge ◽

Domain Peptide ◽

Nemo Binding Domain ◽

Dose Dependent

The aim of the present study is to investigate the protective effects and relevant mechanisms exerted by NEMO-binding domain peptide (NBD) against lipopolysaccharide- (LPS-) induced acute lung injury (ALI) in mice. The ALI model was induced by intratracheally administered atomized LPS (5 mg/kg) to BABL/c mice. Half an hour before LPS administration, we treated the mice with increasing concentrations of intratracheally administered NBD or saline aerosol. Two hours after LPS administration, each group of mice was sacrificed. We observed that NBD pretreatment significantly attenuated LPS-induced lung histopathological injury in a dose-dependent manner. Western blotting established that NBD pretreatment obviously attenuated LPS-induced IκB-αand NF-κBp65 activation and NOX1, NOX2, and NOX4 overexpression. Furthermore, NBD pretreatment increased SOD and T-AOC activity and decreased MDA levels in lung tissue. In addition, NBD also inhibited TNF-αand IL-1βsecretion in BALF after LPS challenge. In conclusion, NBD protects against LPS-induced ALI in mice.

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