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

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