scholarly journals Spilanthes acmella inhibits inflammatory responses via inhibition of NF-κB and MAPK signaling pathways in RAW 264.7 macrophages

2017 ◽  
Vol 16 (1) ◽  
pp. 339-346 ◽  
Author(s):  
Young-Chang Cho ◽  
Tran The Bach ◽  
Ba Reum Kim ◽  
Huong Lan Vuong ◽  
Sayeon Cho
2016 ◽  
Vol 7 (2) ◽  
pp. 1002-1013 ◽  
Author(s):  
Weicheng Hu ◽  
Xinfeng Wang ◽  
Lei Wu ◽  
Ting Shen ◽  
Lilian Ji ◽  
...  

In vitro and in vivo anti-inflammatory activities of apigenin-7-O-β-d-glucuronide.


2018 ◽  
Vol 19 (7) ◽  
pp. 2027 ◽  
Author(s):  
Jingyu He ◽  
Xianyuan Lu ◽  
Ting Wei ◽  
Yaqian Dong ◽  
Zheng Cai ◽  
...  

Hedyotis diffusa is a folk herb that is used for treating inflammation-related diseases in Asia. Previous studies have found that iridoids in H. diffusa play an important role in its anti-inflammatory activity. This study aimed to investigate the anti-inflammatory effect and potential mechanism of five iridoids (asperuloside (ASP), asperulosidic acid (ASPA), desacetyl asperulosidic acid (DAA), scandoside methyl ester (SME), and E-6-O-p-coumaroyl scandoside methyl ester (CSME)) that are presented in H. diffusa using lipopolysaccharide (LPS)—induced RAW 264.7 cells. ASP and ASPA significantly decreased the production of nitric oxide (NO), prostaglandin E2 (PGE2), tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) in parallel with the inhibition of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), TNF-α, and IL-6 mRNA expression in LPS-induced RAW 264.7 cells. ASP treatment suppressed the phosphorylation of the inhibitors of nuclear factor-kappaB alpha (IκB-α), p38, extracellular signal-regulated kinase (ERK), and c-Jun N-terminal kinase (JNK). The inhibitory effect of ASPA was similar to that of ASP, except for p38 phosphorylation. In summary, the anti-inflammatory effects of ASP and ASPA are related to the inhibition of inflammatory cytokines and mediators via suppression of the NF-κB and mitogen-activated protein kinase (MAPK) signaling pathways, which provides scientific evidence for the potential application of H. diffusa.


2006 ◽  
Vol 8 (6) ◽  
pp. 1440-1449 ◽  
Author(s):  
Pei-Jane Tsai ◽  
Ying-Huei Chen ◽  
Chieh-Hsing Hsueh ◽  
Hsiao-Chun Hsieh ◽  
Ya-Hui Liu ◽  
...  

2014 ◽  
Vol 306 (2) ◽  
pp. L183-L195 ◽  
Author(s):  
Hong Pan ◽  
Yijuan Zhang ◽  
Zichao Luo ◽  
Ping Li ◽  
Lanlan Liu ◽  
...  

Since avian influenza virus H5N1-induced hypercytokemia plays a key role in acute lung injury, understanding its molecular mechanism is highly desirable for discovering therapeutic targets against H5N1 infection. In the present study, we investigated the role of autophagy in H5N1-induced lung inflammation by using H5N1 pseudotyped viral particles (H5N1pps). The results showed that H5N1pps significantly induced autophagy both in A549 human lung epithelial cells and in mouse lung tissues, which was primarily due to hemagglutinin (HA) of H5N1 virus. Blocking autophagy with 3-methyladenine (an autophagy inhibitor) or siRNA knockdown of autophagy-related genes ( beclin1 and atg5) dramatically attenuated H5N1pp-induced proinflammatory cytokines and chemokines, such as IL-1β, TNF-α, IL-6, CCL2, and CCL5, both in vitro and in vivo. Autophagy-mediated inflammatory responses involved the activation of NF-κB and p38 MAPK signaling pathways, which required the presence of clathrin but did not rely on p62 or autophagosome-lysosome fusion. On the other hand, the activation of NF-κB also promoted H5N1pp-induced autophagosome formation. These data indicated a positive feedback loop between autophagy and NF-κB signaling cascade, which could exacerbate H5N1pp-induced lung inflammation. Our data demonstrated an essential role of autophagy in H5N1pp-triggered inflammatory responses, and targeting the autophagic pathway could be a promising strategy to treat H5N1 virus-caused lung inflammation.


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