Abstract
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 therapeutic effect on UC. However, the protective mechanism of DRE against UC remains unknown. To discover the targeting pathway involved in DRE-induced protection against UC. 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. 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. The DRE-H is capable of relieving DSS-induced UC, and its mechanism links to the MAPK pathways.
Highlights
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
We found that Dandelion root extracts (DRE)-H attenuated DSS-triggered colonic mucosal damage
The DRE-H is capable of relieving DSS-induced UC, and its mechanism links to the mitogen-activated protein kinases (MAPK) pathways
Summary
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. It has long been known that dandelion (Taraxacum, Asteraceae family), a traditional Chinese herbal medicine, together with other herbs, can treat various ailments.[5] Recent attempts have led to discoveries of anticancer, antiinflammatory and antioxidative functions of this plant.[6,7,8] By stimulating multiple death signaling pathways, the dandelion root extracts increase cell apoptosis of colorectal and pancreatic cancer and leukemia.[9,10,11] Inhibiting PI3K/ AKT pathway is a mechanism for dandelion root extracts to ameliorate lipopolysaccharide (LPS)-triggered inflammation,[12] and reducing lipid peroxidation contributes to the antioxidative activity of dandelion root extracts on the alcohol-induced liver.[13] the protective effect of this plant on UC has been revealed,[14] the exact mechanism is unknown Such a broad function of dandelion root extract might be due to its active chemical constituents, including sesquiterpenes, various triterpenes, phytosterols, and phenolic compounds.[15] Among the phenolic compounds, hydroxycinnamic acid derivatives (chlorogenic, caffeic, 4-coumaric, 3-coumaric, ferulic acids) are mainly reported, whereas flavonoids and hydroxybenzoic acid derivatives have a relatively low level.[16,17,18] These chemical constituents likely act individually, additively or in synergy, in order to modulate different tissue-specific functions.[19] Still, the physiological functions of dandelion and its clinical utilization clues the ability of cells to respond to its bioactive components through fundamental and widespread intracellular mechanisms
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