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Qing Hua Chang Yin attenuates lipopolysaccharide-induced inflammatory response in human intestinal cells by inhibiting NF-κB activation
Ulcerative colitis (UC) is a major form of inflammatory bowel disease (IBD), which is tightly regulated by the nuclear factor κB (NF-κB) pathway. Thus, the suppression of NF-κB signaling may provide a promising strategy for the treatment of UC. Qing Hua Chang Yin (QHCY) is a traditional Chinese form...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2013
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3735875/ https://www.ncbi.nlm.nih.gov/pubmed/23935744 http://dx.doi.org/10.3892/etm.2013.1071 |
Sumario: | Ulcerative colitis (UC) is a major form of inflammatory bowel disease (IBD), which is tightly regulated by the nuclear factor κB (NF-κB) pathway. Thus, the suppression of NF-κB signaling may provide a promising strategy for the treatment of UC. Qing Hua Chang Yin (QHCY) is a traditional Chinese formulation, which has been used for a number of years to clinically treat UC. However, little is known with regard to its anti-inflammatory properties. In the present study, lipopolysaccharide (LPS)-stimulated Caco-2 cells were used as an in vitro inflammatory model of the human intestinal epithelium to evaluate the anti-inflammatory effects of QHCY and its underlying molecular mechanisms. We observed that QHCY inhibited the inflammatory response in intestinal epithelial cells as it significantly and concentration-dependently reduced the LPS-induced secretion of pro-inflammatory TNF-α and IL-8 in Caco-2 cells. Furthermore, QHCY treatment inhibited the phosphorylation of IκB and the nuclear translocation of NF-κB in Caco-2 cells in a concentration-dependent manner, indicating that QHCY suppressed the activation of the NF-κB signaling pathway. Collectively, our results suggest that the inhibition of NF-κB-mediated inflammation may constitute a potential mechanism by which QHCY treats UC. |
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