ArticleFrontiers in immunology2019
FA-97, a New Synthetic Caffeic Acid Phenethyl Ester Derivative, Ameliorates DSS-Induced Colitis Against Oxidative Stress by Activating Nrf2/HO-1 Pathway.
Article in Frontiers in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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37 citing papers in PubMed, 56 citations in OpenAlex.
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- S100A9 deletion ameliorates acute lung injury by attenuating excessive neutrophil activation via activating the NRF2/HO-1 signaling axis.Respiratory research · 2026Article
- Dauricine ameliorates intestinal inflammation and oxidative stress in DSS-induced colitis through TLR4/NLRP3/GSDMD-mediated pyroptosis and Nrf2 pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
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- Antioxidant Therapy in Inflammatory Bowel Diseases: How Far Have We Come and How Close Are We?Antioxidants (Basel, Switzerland) · 2024Review
- Glucocorticoid efficacy and treatment strategies for drug-induced liver injury: a literature review.Molecular biology reports · 2024Review
- Advances in research on immunocyte iron metabolism, ferroptosis, and their regulatory roles in autoimmune and autoinflammatory diseases.Cell death & disease · 2024Review
- Therapeutic effects of genistein in experimentally induced ulcerative colitis in rats via affecting mitochondrial biogenesis.Molecular and cellular biochemistry · 2024Article
- Moxibustion Regulates the BRG1/Nrf2/HO-1 Pathway by Inhibiting MicroRNA-222-3p to Prevent Oxidative Stress in Intestinal Epithelial Cells in Ulcerative Colitis and Colitis-Associated Colorectal Cancer.Journal of immunology research · 2024Article
- Harnessing the Anti-Inflammatory Properties of Polyphenols in the Treatment of Inflammatory Bowel Disease.International journal of biological sciences · 2024Review
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- Biological Activities of p-Hydroxycinnamic Acids in Maintaining Gut Barrier Integrity and Function.Foods (Basel, Switzerland) · 2023Article
- Sodium Butyrate Inhibits Oxidative Stress and NF-κB/NLRP3 Activation in Dextran Sulfate Sodium Salt-Induced Colitis in Mice with Involvement of the Nrf2 Signaling Pathway and Mitophagy.Digestive diseases and sciences · 2023Article
- Sinigrin Attenuates the Dextran Sulfate Sodium-induced Colitis in Mice by Modulating the MAPK Pathway.Inflammation · 2023Article
- Oxidative stress, hormones, and effects of natural antioxidants on intestinal inflammation in inflammatory bowel disease.Frontiers in endocrinology · 2023Review
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inflammatory bowel disease (IBD) is a chronic idiopathic inflammatory disorder of gastro-intestinal tract, lacking effective drug targets and medications. Caffeic acid phenethyl ester (CAPE), a phenolic constituent derived from propolis, has been reported to be a potential therapeutic agent for IBD with low water solubility and poor bioavailability. In this study, we synthesized a new CAPE derivative (FA-97) and aimed to investigate the effect of FA-97 on DSS-induced colitis. Here, we found that FA-97 attenuated body weight loss, colon length shortening and colonic pathological damage in colitis mice, as well as inhibited inflammatory cell infiltration and expression of pro-inflammatory cytokines in colons. In addition, FA-97 reduced ROS production and MDA generation, while total antioxidant capacity both in DSS-induced colitis mice and LPS-stimulated primary BMDMs and RAW 264.7 cells were enhanced. Mechanically, FA-97 activated Nrf2 followed by increased HO-1 and NQO-1 and down-regulated nuclear levels of p65 and c-Jun, to suppress DSS-induced colonic oxidative stress. Moreover, FA-97 decreased pro-inflammatory cytokine expression and increased the antioxidant defenses in RAW 264.7 via Nrf2 activation. In general, this study reveals that FA-97 activates Nrf2/HO-1 pathway to eventually alleviate DSS-induced colitis against oxidative stress, which has potential activity and may serve as a candidate for IBD therapy.
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