Qing Hua Chang Yin exerts therapeutic effects against ulcerative colitis through the inhibition of the TLR4/NF‑κB pathway

Ke,Xiao; Zhou,Fan; Gao,Youliang; Xie,Bingying; Hu,Guanghong; Fang,Wenyi; Peng,Jun; Chen,Youqin; Sferra,Thomas J.

doi:10.3892/ijmm.2013.1458

Qing Hua Chang Yin exerts therapeutic effects against ulcerative colitis through the inhibition of the TLR4/NF‑κB pathway

Authors:
- Xiao Ke
- Fan Zhou
- Youliang Gao
- Bingying Xie
- Guanghong Hu
- Wenyi Fang
- 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, Fujian 350003, P.R. China, Fujian Institute of Chinese Medicine, Fuzhou, Fujian 350003, P.R. China, Academy of Integrative Medicine, Fujian University of Traditional Chinese Medicine, 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: July 29, 2013 https://doi.org/10.3892/ijmm.2013.1458
Pages: 926-930

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Abstract

The activation of the Toll‑like receptor 4 (TLR4)/nuclear factor‑κB (NF‑κB) pathway has been implicated as a key mediator in the pathogenesis of ulcerative colitis (UC); therefore, it has become an attractive target for the treatment of UC. Qing Hua Chang Yin (QHCY) is a traditional Chinese formula, which has been used for many years to clinically treat conditions associated with inflammatory bowel diseases, such as UC. However, the precise mechanisms behind its anti‑inflammatory effects remain largely unknown. In this study, using the dextran sulfate sodium (DSS)‑induced colitis mouse model, we evaluated the therapeutic effects of QHCY against UC and elucidated the possible underlying molecular mechanisms. We found that the administration of QHCY profoundly ameliorated DSS‑induced clinical manifestations, colon shortening and histological damage in the mice with colitis. In addition, treatment with QHCY significantly decreased the DSS‑induced secretion of serum amylase. Moreover, QHCY significantly inhibited the DSS‑induced expression of TLR4 and myeloid differentiation primary response gene 88 (MyD88), the phosphorylation of IκB and the nuclear translocation of NF‑κB. Taken together, our findings suggest that the suppression of the TLR4/NF‑κB signaling pathway may be one of the mechanisms involved in the therapeutic effects of QHCY against UC.

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