Umbelliferone attenuates lipopolysaccharide-induced acute lung injury linked with regulation of TLRs–MyD88 and RIP140/NF-κB signaling pathways

RSC Advances ◽  
2016 ◽  
Vol 6 (100) ◽  
pp. 97503-97511 ◽  
Author(s):  
Fen Luo ◽  
Rui Zhou ◽  
Hui Lei ◽  
Yi Mou ◽  
Ping Zhang ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Signaling Pathways ◽  
Chloroform Fraction ◽  
Pharmacological Activities

Umbelliferone (Umb), isolated from the chloroform fraction of Potentilla evestita, exerts a variety of pharmacological activities.

Cardamine komarovii flower extract reduces lipopolysaccharide-induced acute lung injury by inhibiting MyD88/TRIF signaling pathways

2019 ◽  
Vol 17 (6) ◽  
pp. 461-468
Author(s):  
Qi CHEN ◽  
Ke-Xin ZHANG ◽  
Tai-Yuan LI ◽  
Xuan-Mei PIAO ◽  
Mei-Lan LIAN ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Signaling Pathways ◽  
Flower Extract

Protective effects of pogostone against LPS-induced acute lung injury in mice via regulation of Keap1–Nrf2/NF-κB signaling pathways

2016 ◽  
Vol 32 ◽  
pp. 55-61 ◽  
Author(s):  
Chao-Yue Sun ◽  
Lie-Qiang Xu ◽  
Zhen-Biao Zhang ◽  
Chao-hui Chen ◽  
Yong-zhong Huang ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Signaling Pathways ◽  
Protective Effects

scholarly journals Angelica Polysaccharide Ameliorates Sepsis-Induced Acute Lung Injury through Inhibiting NLRP3 and NF-κB Signaling Pathways in Mice

2021 ◽  
Vol 2021 ◽  
pp. 1-9
Author(s):  
Yan Zhu ◽  
Taocheng Meng ◽  
Aichen Sun ◽  
Jintao Li ◽  
Jinlai Li
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Signaling Pathways ◽  
Cecal Ligation ◽  
Weight Ratio ◽  
Receptor Protein ◽  
Lung Edema ◽  
Caspase 1 ◽  
Tnf Α

Objective. This study aimed to explore the role of angelica polysaccharide (AP) in sepsis-induced acute lung injury (ALI) and its underlying molecular mechanism. Methods. A sepsis model of cecal ligation and puncture (CLP) in male BALB/C mice was used. Then, 24 h after CLP, histopathological changes in lung tissue, lung wet/dry weight ratio, and inflammatory cell infiltration were analyzed. Next, levels of inflammatory cytokines (tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, IL-6, and IL-18), as well as the activity of myeloperoxidase (MPO), malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione (GSH), were measured to assess the role of AP. The protein expression of NF-κB p65, p-NF-κB p65, IκBα, p-IκBα, nucleotide-binding domain- (NOD-) like receptor protein 3 (NLRP3), ASC, and caspase-1 was detected by western blot. In addition, the expression of p-NF-κB p65 and NLRP3 was detected by immunohistochemistry. Results. AP treatment ameliorated CLP-induced lung injury and lung edema, as well as decreased the number of total cells, neutrophils, and macrophages in bronchoalveolar lavage fluid (BALF). AP reduced the levels of TNF-α, IL-1β, IL-6, and IL-18 in BALF, as well as in serum. Moreover, AP decreased MPO activity and MDA content, whereas increased SOD and GSH levels. AP inhibited the expression of p-NF-κB p65, p-IκBα, NLRP3, ASC, and caspase-1, while promoted IκBα expression. Conclusion. This study demonstrated that AP exhibits protective effects against sepsis-induced ALI by inhibiting NLRP3 and NF-κB signaling pathways in mice.

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