scholarly journals Glutamine ameliorates lipopolysaccharide‑induced cardiac dysfunction by regulating the toll‑like receptor 4/mitogen‑activated protein kinase/nuclear factor‑kB signaling pathway

2017 ◽  
Author(s):  
Wen‑Bin Zhang ◽  
Hai‑Yue Zhang ◽  
Qian Zhang ◽  
Fang‑Zhou Jiao ◽  
Hong Zhang ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Signaling Pathway ◽  
Cardiac Dysfunction ◽  
Mitogen Activated Protein Kinase ◽  
Nuclear Factor ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Mitogen Activated Protein ◽  
Nuclear Factor Kb

scholarly journals The anti-inflammatory effect and potential mechanism of cardamonin in DSS-induced colitis

2015 ◽  
Vol 309 (7) ◽  
pp. G517-G527 ◽  
Author(s):  
Gaiyan Ren ◽  
Aning Sun ◽  
Chao Deng ◽  
Jingjing Zhang ◽  
Xiaojun Wu ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Protein Kinase ◽  
Bowel Disease ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Mitogen Activated Protein Kinase ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Mitogen Activated Protein ◽  
Inflammatory Bowel

Cardamonin is a naturally occurring chalcone with strong anti-inflammatory activity. However, the direct effect of cardamonin on intestinal inflammation remains elusive. In the present study, we found that cardamonin markedly ameliorated dextran sulfate sodium-induced mouse body weight loss, diarrhea, colon shortening, spleen swelling, and histological damage, which correlated with a decline in the activity of myeloperoxidase and the production of nitric oxide, tumor necrosis factor-α and interleukin-6 in the colon. The upregulation of toll-like receptor 4 after dextran sulfate sodium treatment was associated with an increase in the activation of myeloid differentiation factor 88, interleukin-1 receptor-associated kinase-1, nuclear factor-κB (NF-κB) p65, inhibitor κBα, and inhibitor κB kinase-α/β, as well as the mitogen-activated protein kinase molecules of extracellular signal-regulated kinase and c-Jun NH2-terminal kinase, and this upregulation was reversed by cardamonin administration. Moreover, cardamonin blocked the nuclear translocation of NF-κB p65, inhibited NF-κB-luciferase activity, and downregulated NF-κB target genes expression. The present study clearly demonstrates a beneficial effect of cardamonin on experimental inflammatory bowel disease via a mechanism associated with suppression of toll-like receptor 4 expression and inactivation of NF-κB and mitogen-activated protein kinase pathways. This study may give insight into the further evaluation of the therapeutic potential of cardamonin or its derivatives for human inflammatory bowel disease.

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