ArticleDrug design, development and therapy2025
Preventive Effect of Oleanolic Acid on Ulcerative Colitis Caused by Dextran Sulfate Sodium via a PPARγ-Involved Mechanism in Mice.
Article in Drug design, development and therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- Stemness-associated MEF-derived extruded nanovesicles cooperate withNanoscale advances · 2026Article
- Self-Assembled Carrier-Free Nanostructures of Anemoside B4 and Oleanolic Acid Alleviate Intestinal Injury Induced by IntraperitonealAntioxidants (Basel, Switzerland) · 2026Article
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: Oleanolic acid (OA), a naturally occurring pentacyclic triterpenoid, has been reported to possess anti-inflammatory and barrier-protective properties. However, its molecular mechanism in the context of ulcerative colitis (UC) remains unclear. Methods: In this study, we evaluated the therapeutic potential of OA (25 and 50 mg/kg/day) in a dextran sulfate sodium (DSS)-induced acute colitis model in C57BL/6 mice. Results: Oral administration of OA significantly alleviated clinical symptoms of colitis, including weight loss, colon shortening, increased disease activity index (DAI), and histopathological injury. Additionally, OA demonstrated potent anti-inflammatory effects by suppressing the production of pro-inflammatory cytokines and promoting anti-inflammatory cytokines. It also restored redox homeostasis by enhancing antioxidant defenses and reducing lipid peroxidation. OA also restored intestinal barrier integrity, as evidenced by increased tight junction protein expression and decreased intestinal permeability. Mechanistically, OA was found to inhibit the activation of the NF-κB signaling pathway, as evidenced by reduced phosphorylation of IKKα/β and p65, and decreased degradation of IκBα. A key finding was that OA restored the expression of PPARγ, a known negative regulator of NF-κB. OA promoted the accumulation of peroxisome proliferator-activated receptor gamma (PPARγ), a nuclear receptor essential for maintaining intestinal epithelial homeostasis and anti-inflammatory signaling. OA inhibited the ubiquitin-mediated proteasomal degradation of PPARγ, thereby stabilizing its protein levels in colonic tissue. Pharmacological inhibition of PPARγ with GW9662 abolished the protective effects of OA on intestinal inflammation and epithelial barrier function, confirming that PPARγ activation is required for OA-mediated protection. Conclusion: These findings identify a previously unrecognized mechanism whereby OA protects against colitis through post-translational stabilization of PPARγ. Our study not only highlights the therapeutic value of OA as a potential intervention for UC but also provides mechanistic insight into the regulation of nuclear receptor homeostasis during intestinal inflammation.
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