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Updated: Feb 26, 2026
Murine Colitis Modeling using Dextran Sulfate Sodium DSS
Published on: January 19, 2010
Cideb Deficiency Aggravates Dextran Sulfate Sodium-induced Ulcerative Colitis in Mice by Exacerbating the Oxidative
Chao Sun1, Yuanlin Zhao, Xing Gao
1*State Key Laboratory of Cancer Biology and Department of Pathology, Xijing Hospital, the Fourth Military Medical University, Xi'an, China; †Department of Neurology, Tangdu Hospital, the Fourth Military Medical University, Xi'an, China; ‡Department of Pathology, Chengdu Military General Hospital, Chengdu, China; §Department of Clinical Laboratory, Tangdu Hospital, the Fourth Military Medical University, Xi'an, China; ‖Department of Neurology, Shaanxi People Hospital, Xi'an, China; ¶Department of Pathology, Basic Medicine and School of Basic Medical Sciences, Xi'an Medical University, Xi'an, China; **Department of Cardiology, Xijng Hospital, the Fourth Military Medical University, Xi'an, China; and ††Department of Ultrasonography, Xijng Hospital, the Fourth Military Medical University, Xi'an, China.
Background:
Abnormal lipid metabolism is one of many factors that contribute to the development of ulcerative colitis (UC). As a lipid droplet-associated protein, Cideb facilitated the export of lipids from enterocytes and promoted intestinal lipid absorption. We found that Cideb was upregulated in the colonic mucosa of both UC patients and dextran sodium sulfate (DSS)-induced mouse colitis, but its roles in the pathogenesis of UC are still ill-defined.
Methods:
Acute colitis was induced with DSS in Cideb-null and wild-type mice, and the inflammation and oxidative stress were evaluated in the colonic mucosa. Moreover, triglyceride accumulation and oxidative stress were further analyzed in polarized Caco-2 cells with overexpression of Cideb.
Results:
Our present data indicated that Cideb-null mice were more susceptible to DSS-induced colitis, and consumption of a high-fat diet exacerbated the deterioration of DSS-induced colitis in Cideb-null mice. Moreover, Cideb deficiency increased the colonic oxidative stress in DSS-treated mice and more significant under a high-fat diet condition. In exploring the mechanism, we found that Cideb deficiency elevated the lipid content in both feces and the colonic mucosa of DSS-treated mice, especially those fed with a high-fat diet. The in vitro evidence proved that Cideb expression reduced triglyceride accumulation and oxidative stress in polarized Caco-2 cells in the presence of oleic acid.
Conclusions:
Our data suggest that Cideb plays a protective role against the development of UC by reducing the lipid accumulation and oxidative damage in the colonic mucosa. Therefore, Cideb could be a potential therapeutic target for UC.
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