期刊
EUROPEAN JOURNAL OF PHARMACOLOGY
卷 911, 期 -, 页码 -出版社
ELSEVIER
DOI: 10.1016/j.ejphar.2021.174518
关键词
Ulcerative colitis; Inflammation; Astragalus polysaccharide; Ferroptosis; NRF2
资金
- National Natural Science Founda-tion of China [82073156, 81802843]
- Suzhou Science & Technology plan project [SYS2019035]
- Natural Science Foundation of the Jiangsu Higher Education Institutions of China [20KJA310005]
- Key Project of Medical Research of Jiangsu Commission of Health [ZDA2020008]
- Post-graduate Research & Practice Innovation Program of Jiangsu Province [KYCX21_2970]
Astragalus polysaccharide (APS) demonstrated its ability to prevent ferroptosis in a murine model of experimental colitis and human Caco-2 cells by inhibiting the NRF2/HO-1 pathway.
Ulcerative colitis (UC) is a relapsing and remitting inflammatory bowel disease (IBD), but current conventional drugs lack efficacy. Astragalus polysaccharide (APS) is an active ingredient of Astragalus membranaceus and has been shown to ameliorate experimental colitis. In the present study, we aimed to investigate how APS affects the ferroptosis of intestinal epithelial cells in dextran sulfate sodium (DSS)-induced experimental colitis in mice. Our data showed that APS administration attenuated total weight loss, colon length shortening, disease activity index (DAI) scores, histological damage, and the expression of inflammatory cytokines in the colon of DSS-challenged mice. Moreover, we observed that treatment with APS obviously inhibited ferroptosis in both DSS-challenged mice and RSL3-stimulated Caco-2 cells, as indicated by the decrease in the expression of ferroptosis-associated genes (PTGS2, FTH, and FTL) and the levels of surrogate ferroptosis markers (MDA, GSH, and iron load). Mechanistically, the inhibitory effects of APS on ferroptosis in DSS-challenged mice and RSL3-stimulated Caco-2 cells were associated with the NRF2/HO-1 pathway. Collectively, our findings identify a new role of APS in preventing ferroptosis in a murine model of experimental colitis and human Caco-2 cells via inhibiting NRF2/ HO-1 pathway.
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