Tectorigenin inhibits inflammatory responses in murine inflammatory bowel disease and LPS‐stimulated macrophages via inactivating MAPK signaling pathway

Author:

Huang Hong1,Tang Sanhui1,Zhou Yanghong1,Cai Yi2ORCID

Affiliation:

1. Department of TCM and Integrated TCM and Western Medicine Hunan Provincial People's Hospital, The First Affiliated Hospital of Hunan Normal University Changsha China

2. Department of Liver and Gall Surgical Hunan Provincial People's Hospital, The First Affiliated Hospital of Hunan Normal University Changsha China

Abstract

AbstractBackgroundConsidering the antihepatitis effects of Tectorigenin (TEC), and the same adenosine mitogen‐activated protein kinase (MAPK) pathway in both hepatitis and inflammatory bowel disease (IBD) models, exploring the role of TEC in IBD is contributive to develop a new treatment strategy against IBD.MethodsThe IBD mouse model was constructed by feeding with dextran sodium sulfate (DSS) and injection of TEC. Afterward, the mouse body weight, colon length, and disease activity index (DAI) were tested to assess the enteritis level. Mouse intestine lesions were detected by hematoxylin and eosin staining. Murine macrophages underwent lipopolysaccharide (LPS) induction to establish an inflammation model. Cell viability was determined by cell counting kit‐8 assay. Enzyme‐linked immunosorbent assay was performed to measure interleukin 6 (IL‐6) and tumor necrosis factor‐α (TNF‐α) levels. Cyclooxygenase‐2 (COX‐2) and inducible nitric oxide synthase (iNOS) expressions were quantified via quantitative reverse transcription polymerase chain reaction. Levels of MAPK pathway‐related proteins (p‐P38, P38, p‐Jun N‐terminal kinase (JNK), JNK, signal‐regulated kinase (ERK), p‐ERK), COX‐2 and iNOS were quantitated by Western blot.ResultsTEC improved the inflammatory response through ameliorating weight loss, shortening colon, and increasing DAI score in IBD mouse. Expressions of intestinal inflammatory factors (IL‐6, TNF‐α, iNOS and COX‐2) and MAPK pathway‐related proteins (p‐P38, p‐JNK, and p‐ERK) were increased both in DSS‐induced mouse intestinal tissue, but TEC inhibited expressions of inflammatory factors. The same increased trend was identified in LPS‐induced macrophages, but TEC improved macrophage inflammation, as evidenced by downregulation of inflammatory factors.ConclusionTEC mitigates IBD and LPS‐induced macrophage inflammation in mice via inhibiting MAPK signaling pathway.

Publisher

Wiley

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