scholarly journals Anti-neuroinflammatory activity of Humulus japonicus extract and its active compound luteolin on lipopolysaccharide-induced inflammatory response in SIM-A9 microglia via NF-κB and MAPK signaling pathways

2021 ◽  
Author(s):  
Feng WANG ◽  
Byoung Ok CHO ◽  
Jae Young SHIN ◽  
Suping HAO ◽  
Seon Il JANG
Keyword(s):  
Inflammatory Response ◽  
Signaling Pathways ◽  
Active Compound ◽  
Mapk Signaling ◽  
Humulus Japonicus ◽  
Mapk Signaling Pathways

Inducing inflammatory response in RAW264.7 and NK-92 cells by an arabinogalactan isolated from Ferula gummosa via NF-κB and MAPK signaling pathways

2020 ◽  
Vol 241 ◽  
pp. 116358
Author(s):  
Mehdi Tabarsa ◽  
Elham Hashem Dabaghian ◽  
SangGuan You ◽  
Khamphone Yelithao ◽  
Subramanian Palanisamy ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Signaling Pathways ◽  
Mapk Signaling ◽  
Mapk Signaling Pathways

Artemisinin inhibits inflammatory response via regulating NF-κB and MAPK signaling pathways

2016 ◽  
Vol 39 (1) ◽  
pp. 28-36 ◽  
Author(s):  
Ke Si Wang ◽  
Junbo Li ◽  
Zhe Wang ◽  
Chunliu Mi ◽  
Juan Ma ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Signaling Pathways ◽  
Mapk Signaling ◽  
Mapk Signaling Pathways

scholarly journals E3 ligase TRIM47 positively regulates endothelial activation and pulmonary inflammation through potentiating the K63-linked ubiquitination

2021 ◽  
Author(s):  
Yisong Qian ◽  
Ziwei Wang ◽  
Hongru Lin ◽  
Tianhua Lei ◽  
Zhou Zhou ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Inflammatory Response ◽  
Signaling Pathways ◽  
Pulmonary Inflammation ◽  
Endothelial Activation ◽  
Mapk Signaling ◽  
Monocyte Adhesion ◽  
Mapk Signaling Pathways

Endothelial activation plays an essential role in the pathology of sepsis-induced acute lung injury, but the detailed regulatory mechanisms remain largely unknown. Here, we demonstrated that TRIM47, an ubiquitin E3 ligase of tripartite protein family, is highly expressed in vascular endothelial cells and is up-regulated during TNFα-induced endothelial activation. Knockdown of TRIM47 in endothelial cells prevents the transcription of multiple pro-inflammatory cytokines, reduces monocyte adhesion and the expression of adhesion molecules, and inhibits the secretion of IL-1β and IL-6 into the supernatant. By contrast, overexpression of TRIM47 promotes inflammatory response and monocyte adhesion upon TNFα stimulation. TRIM47 modulates the activation of NF-κB and MAPK signaling pathways during endothelial activation. Further experiment confirmed that TRIM47 interacts with TRAF2 and mediates K63-linked ubiquitination. In addition, TRIM47-deficient mice are more resistant to lipopolysaccharide-induced acute lung injury and death, due to attenuated pulmonary inflammation. Taken together, our studies suggest that TRIM47 promotes pulmonary inflammation and injury at least partly through potentiating the K63-linked ubiquitination of TRAF2, which in turn activates NF-κB and MAPK signaling pathways to trigger inflammatory response in endothelial cells.

Sign in / Sign up

Export Citation Format

Share Document