Dandelion root extracts abolish MAPK pathways to ameliorate experimental mouse ulcerative colitis

<p>Abstract<br> Background. Dextran sodium sulfate (DSS)-triggered ulcerative colitis (UC) model in animals provides<br> a valuable platform to preclinically evaluate the outcome of drug candidates for UC. Dandelion root extracts<br> (DRE) have a particular therapeutic effect on UC. However, the protective mechanism of DRE against UC<br> remains unknown.<br> Objectives. To discover the targeting pathway involved in DRE-induced protection against UC.<br> Materials and methods. The UC model was developed in C57BL/6 mice by oral administration of DSS.<br> Following DSS exposure, sulfasalazine (SASP), low dose of DRE (DRE-L), moderate dose of DRE (DRE-M), high<br> dose of DRE (DRE-H), and DRE-H plus mitogen-activated protein kinases (MAPK) agonist (DRE-H+MA) were<br> administered to the mice. Colon Mucosal Damage Index (CMDI) and histopathological analysis were used<br> to evaluate the colonic mucosal damage. The cytokine levels were detected using commercial enzyme-linked<br> immunosorbent assay (ELISA) kits. The MAPK pathway activation was determined with western blotting.<br> Results. We found that DRE-H attenuated DSS-triggered colonic mucosal damage. The DSS-induced inflammatory responses and oxidative stress in the bloodstream and colon tissues were dramatically inhibited<br> by DRE-H administration. Also, this plant impaired DSS-provoked phosphorylation levels of extracellular<br> signal-regulated kinases (ERK), c-Jun N-terminal kinases (JNK), p38 mitogen-activated protein kinases<br> (p38), p65, and I&kappa;B. More importantly, MAPK agonist, BIM-23A760, removed the protective effect of DRE-H<br> on the bloodstream and colon tissues.<br> Conclusions. The DRE-H is capable of relieving DSS-induced UC, and its mechanism links to the MAPK<br> pathways.<br> &nbsp;</p>