title: Qing Hua Chang Yin exerts therapeutic effects against ulcerative colitis through the inhibition of the TLR4/NF-κB pathway.
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.
authors.affiliation: Department of Gastroenterology, Second Affiliated Hospital of Fujian University of Traditional Chinese Medicine, Fujian 350003, PR China. drkxkx@163.com
authors.forename: Xiao
authors.initials: X
authors.lastname: Ke
authors.forename: Fan
authors.initials: F
authors.lastname: Zhou
authors.forename: Youliang
authors.initials: Y
authors.lastname: Gao
authors.forename: Bingying
authors.initials: B
authors.lastname: Xie
authors.forename: Guanghong
authors.initials: G
authors.lastname: Hu
authors.forename: Wenyi
authors.initials: W
authors.lastname: Fang
authors.forename: Jun
authors.initials: J
authors.lastname: Peng
authors.forename: Youqin
authors.initials: Y
authors.lastname: Chen
authors.forename: Thomas J
authors.initials: TJ
authors.lastname: Sferra
mesh_terms: D000818:Animals; D003093:Colitis, Ulcerative / Q000139:chemically induced / Q000188:drug therapy* / Q000235:genetics; D003106:Colon / Q000187:drug effects / Q000473:pathology; D016264:Dextran Sulfate / Q000009:adverse effects; D004195:Disease Models, Animal; D020672:I-kappa B Proteins / Q000235:genetics / Q000378:metabolism; D008297:Male; D008516:Medicine, Chinese Traditional; D051379:Mice; D008807:Mice, Inbred BALB C; D053594:Myeloid Differentiation Factor 88 / Q000235:genetics / Q000378:metabolism; D000072000:NF-KappaB Inhibitor alpha; D016328:NF-kappa B / Q000235:genetics* / Q000378:metabolism; D010766:Phosphorylation; D015398:Signal Transduction; D051197:Toll-Like Receptor 4 / Q000235:genetics* / Q000378:metabolism
chemical_list: D020672:I-kappa B Proteins; C507780:Myd88 protein, mouse; D053594:Myeloid Differentiation Factor 88; D016328:NF-kappa B; C000606205:Nfkbia protein, mouse; C493487:Tlr4 protein, mouse; D051197:Toll-Like Receptor 4; D000072000:NF-KappaB Inhibitor alpha; D016264:Dextran Sulfate