Protective effect of sesamol on the pulmonary inflammatory response and lung injury in endotoxemic rats

2010 ◽  
Vol 48 (7) ◽  
pp. 1821-1826 ◽  
Author(s):  
Pei-Yi Chu ◽  
Se-Ping Chien ◽  
Dur-Zong Hsu ◽  
Ming-Yie Liu
Keyword(s):  
Lung Injury ◽  
Inflammatory Response ◽  
Protective Effect ◽  
Pulmonary Inflammatory Response

scholarly journals Emodin alleviates LPS-induced inflammatory response in lung injury rat by affecting the function of neutrophils

2020 ◽  
Author(s):  
Hongxia Mei ◽  
Ying Tao ◽  
Tianhao Zhang ◽  
Feng Qi
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Inflammatory Response ◽  
Rat Model ◽  
Neutrophil Function ◽  
Life Threatening ◽  
Pulmonary Inflammatory Response ◽  
Anti Inflammatory ◽  
Factor Α ◽  
The Impact

Abstract Background: Acute lung injury (ALI) and/or acute respiratory distress syndrome (ARDS) are critical life-threatening syndromes characterized by the infiltration of a large number of neutrophils that lead to an excessive inflammatory response. Emodin (Emo) is a naturally occurring anthraquinone derivative and an active ingredient of Chinese medicine. It is believed to have anti-inflammatory effects. In this study, we examined the impact of Emo on the pulmonary inflammatory response and the neutrophil function in a rat model of lipopolysaccharide (LPS)-induced ALI.Results: Treatment with Emo protected rat against LPS-induced ALI. Compared to untreated rat, Emo-treated rat exhibited significantly ameliorated lung pathological changes and decreased tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β). However, Emo has no protective effect on the rat model of acute lung injury with neutrophil deficiency. In addition, treatment with Emo enhanced the bactericidal capacity of LPS-induced neutrophils via the up-regulation of the ability of neutrophils to phagocytize bacteria and generate neutrophil extracellular traps (NETs). Emo also downregulated the neutrophil respiratory burst and the expression of reactive oxygen species (ROS) in LPS-stimulated neutrophils, alleviating the damage of neutrophils to surrounding tissues. Finally, Emo can accelerate the resolution of inflammation by promoting apoptosis of neutrophils. Conclusion: Our results provide the evidence that Emo could ameliorates LPS-induced ALI via its anti-inflammatory action by modulating the function of neutrophils. Emo may be a promising preventive and therapeutic agent in the treatment of ALI.

miR-138-5p targets sirtuin1 to regulate acute lung injury by regulation of the NF-κB signaling pathway

2020 ◽  
Vol 98 (8) ◽  
pp. 522-530
Author(s):  
Yinshan Wu ◽  
Weiliang Jiang ◽  
Zhuhua Lu ◽  
Wei Su ◽  
Nan Liu ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Inflammatory Response ◽  
Signaling Pathway ◽  
A549 Cells ◽  
Luciferase Assay ◽  
Promote Cell Proliferation ◽  
Pulmonary System ◽  
Pulmonary Inflammatory Response

Acute lung injury (ALI), a disease with a high mortality rate, is a noncardiogenic pulmonary inflammatory response and characterized by damage to the pulmonary system. In this study, we explored the mechanism of the occurrence and development of ALI. It was firstly found that miR-138-5p could inhibit the expression of sirtuin1 (SIRT1), and we further demonstrated that miR-138-5p targets directly SIRT1 through the luciferase assay, while the latter negatively regulated the expression of NF-κB. A549 cells were treated with lipopolysaccharide in vitro to simulate ALI cells and induce ALI in the model mice. The results showed that inhibiting the expression of miR-138-5p could effectively increase the viability of damaged cells, promote cell proliferation, reduce apoptosis, inhibit the inflammatory response, reduce oxidative stress, and then relieve ALI symptoms. Collectively, our results suggested that miR-138-5p can inhibit SIRT1 expression and indirectly activate the NF-κB signaling pathway, thus regulating the development of ALI.

scholarly journals Emodin alleviates LPS-induced inflammatory response in lung injury rat by affecting the function of neutrophils

2020 ◽  
Author(s):  
Hongxia Mei ◽  
Ying Tao ◽  
Tianhao Zhang ◽  
Feng Qi
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Inflammatory Response ◽  
Rat Model ◽  
Neutrophil Function ◽  
Life Threatening ◽  
Pulmonary Inflammatory Response ◽  
Anti Inflammatory ◽  
Factor Α ◽  
The Impact

Abstract Background: Acute lung injury (ALI) and/or acute respiratory distress syndrome (ARDS) are critical life-threatening syndromes characterized by the infiltration of a large number of neutrophils that lead to an excessive inflammatory response. Emodin (Emo) is a naturally occurring anthraquinone derivative and an active ingredient of Chinese medicine. It is believed to have anti-inflammatory effects. In this study, we examined the impact of Emo on the pulmonary inflammatory response and the neutrophil function in a rat model of lipopolysaccharide (LPS)-induced ALI.Results: Treatment with Emo protected rat against LPS-induced ALI. Compared to untreated rat, Emo-treated rat exhibited significantly ameliorated lung pathological changes and decreased tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β). However, Emo has no protective effect on the rat model of acute lung injury with neutrophil deficiency. In addition, treatment with Emo enhanced the bactericidal capacity of LPS-induced neutrophils via the up-regulation of the ability of neutrophils to phagocytize bacteria and generate neutrophil extracellular traps (NETs). Emo also downregulated the neutrophil respiratory burst and the expression of reactive oxygen species (ROS) in LPS-stimulated neutrophils, alleviating the damage of neutrophils to surrounding tissues. Finally, Emo can accelerate the resolution of inflammation by promoting apoptosis of neutrophils. Conclusion: Our results provide the evidence that Emo could ameliorates LPS-induced ALI via its anti-inflammatory action by modulating the function of neutrophils. Emo may be a promising preventive and therapeutic agent in the treatment of ALI.

scholarly journals The β3/5 Integrin-MMP9 Axis Regulates Pulmonary Inflammatory Response and Endothelial Leakage in Acute Lung Injury

2021 ◽  
Vol Volume 14 ◽  
pp. 5079-5094
Author(s):  
Yao Tong ◽  
Chengrong Bao ◽  
Yi-Qiong Xu ◽  
Lei Tao ◽  
Yao Zhou ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Inflammatory Response ◽  
Pulmonary Inflammatory Response
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