ReferenceID 5001

Curculigoside inhibits ferroptosis in ulcerative colitis through the induction of GPX4

Life Sci

Curculigoside (CUR) is natural ingredient from Curculigo orchioides Gaertn with multiple biological activities. However, whether CUR protects from ulcerative colitis (UC) and underlying mechanisms are unclear. Herein, mi

Back to Browse

Relationship Network

Interactive first-hop connections across herbs, ingredients, formulas, targets, diseases, symptoms, syndromes, evidence, and monographs.

Click a node to open it in a new tab
Ingredient: 1Reference: 1Links: 1
Arranging relationship network...

Record Fields

Scalar fields from the final reference record.

Reference Id
5001
Evidence Id
21591
Core Evidence Id
21591
Source Reference Id
3255
Herb2 Reference Id
HBREF004052
Subject Paper Key
HBIN021964_32861798
Pubmed Id
32861798
Doi
10.1016/j.lfs.2020.118356
Paper Title
Curculigoside inhibits ferroptosis in ulcerative colitis through the induction of GPX4
Paper Abstract
Curculigoside (CUR) is natural ingredient from Curculigo orchioides Gaertn with multiple biological activities. However, whether CUR protects from ulcerative colitis (UC) and underlying mechanisms are unclear. Herein, mice challenged with dextran sulfate sodium (DSS) were established and administrated with CUR for 7 days. Then histological pathologies and ferroptosis regulators were determined in vivo. The ferroptotic IEC-6 cells were prepared to investigate the underlying mechanism of CUR. Results showed that CUR inhibited the disease activity index, histological damage and cell death in mice with colitis. We also found that ferroptosis was induced in mice with colitis, as evidenced by iron overload, GSH depletion, ROS and MDA production, accompanied by decreased expression of SOD and GPX4. CUR treatment significantly reversed these alterations of ferroptotic features in DSS-induced mice. Furthermore, similar effects of CUR on ferroptosis were observed in IEC-6 cells under the combined treatment of H2O2 and iron chloride hexahydrate. Interestingly, we found that CUR could increase the selenium sensitivity and promote GPX4 transcription level in IEC-6 cells. Knockdown of GPX4 significantly blocked the protective effects of CUR on cell death, GSH and MDA contents as well as LDH activity in ferroptotic IEC-6 cells. Taken together, these findings suggest that CUR protects against ferroptosis in UC by the induction of GPX4, which presents a potential agent for UC treatment.
Journal
Life Sci
Publish Year
2020
Experiment Subject
mouse; ferroptotic iec-6 cells; iec-6 cells
Experiment Type
Animal & Cell Experiment
Phenotype Related
Ferroptosis; Ulcerative Colitis; Colitis
Paper Title Cn
Paper Title En
Curculigoside inhibits ferroptosis in ulcerative colitis through the induction of GPX4
Bilingual Status
semi_complete