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Albiflorin attenuates inflammation and apoptosis by upregulating AMPK-mediated expression of CDX2 in a mouse model of ulcerative colitis
Abstract
Purpose: To investigate the mechanism underlying the ameliorative effect of albiflorin (AF) on ulcerative colitis (UC) in dextran sulphate sodium (DSS)-induced mice model.
Method: Female C57BL/6 mice were administered DSS to establish a mice model of UC. After one week, the mice received AF, and the body weight and length of colon were measured. The histopathological features of colon tissues treated with hematoxylin-eosin (H & E) stain were examined
by microscopy. Expression of inflammatory cytokines and apoptosis-related proteins were determined using enzyme-linked immunosorbent assay (ELISA) and western blotting.
Results: The relative abundance of goblet cells and crypts of mice were significantly reduced in DSSinduced UC mice model; furthermore, focal ulcers and mucosal damage were apparent. Moreover, treatment with DSS decreased body weight and colon length, downregulated Bcl-2 and AMPK pathwayrelated proteins, increased inflammatory cytokines levels, and upregulated Bax and cleaved caspase-3. In contrast, treatment with AF completely ameliorated DSS-induced effects.
Conclusion: AF treatment attenuated DSS-induced inflammation response and apoptosis via AMPK pathway and modulation of CDX2 expression in UC mice model.
Keyword: Albiflorin, Ulcerative colitis, AMPK, CDX2, Apoptosis
