Qing Hua Chang Yin attenuates lipopolysaccharide-induced inflammatory response in human intestinal cells by inhibiting NF-κB activation

Ke,Xiao; Chen,Jingtuan; Zhang,Xin; Fang,Wenyi; Yang,Chunbo; Peng,Jun; Chen,Youqin; Sferra,Thomas  J.

doi:10.3892/etm.2013.1071

Qing Hua Chang Yin attenuates lipopolysaccharide-induced inflammatory response in human intestinal cells by inhibiting NF-κB activation

Authors:
- Xiao Ke
- Jingtuan Chen
- Xin Zhang
- Wenyi Fang
- Chunbo Yang
- Jun Peng
- Youqin Chen
- Thomas J. Sferra
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Affiliations: Department of Gastroenterology, Second Affiliated Hospital of Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian 350003, P.R. China, Academy of Integrative Medicine, Fujian University of Traditional Chinese Medicine, Minhou Shangjie, Fuzhou, Fujian 350122, P.R. China, Rainbow Babies and Children's Hospital, Case Western Reserve University School of Medicine, Cleveland, OH 44106, USA
Published online on: April 22, 2013 https://doi.org/10.3892/etm.2013.1071
Pages: 189-193

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Abstract

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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