ArticleInflammatory bowel diseases2024
2'-Hydroxycinnamaldehyde Alleviates Intestinal Inflammation by Attenuating Intestinal Mucosal Barrier Damage Via Directly Inhibiting STAT3.
Article in Inflammatory bowel diseases, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- Low-grade mucosal inflammation in aged senescence-accelerated mouse-prone 8 mice blunts epithelial barrier recovery after dextran sodium sulphate-induced chronic colitis.Biogerontology · 2026Article
- Integrated transcriptome and single-cell RNA sequencing identifies small GTPase-associated biomarkers in ulcerative colitis.Frontiers in immunology · 2026Article
- Metformin attenuates colitis via blocking STAT3 acetylation by reducing acetyl-CoA production.Journal of advanced research · 2026Article
- Exploring the beneficial effects of GHK-Cu on an experimental model of colitis and the underlying mechanisms.Frontiers in pharmacology · 2025Article
- Natural products for the treatment of ulcerative colitis: focus on the JAK/STAT pathway.Frontiers in immunology · 2025Review
- Potential applications and mechanisms of natural products in mucosal-related diseases.Frontiers in immunology · 2025Review
- Cinnamic Acid Derivatives as Potential Multifunctional Agents in Cosmetic Formulations Used for Supporting the Treatment of Selected Dermatoses.Molecules (Basel, Switzerland) · 2024Review
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
backgroundThe currently available clinical therapeutic drugs for ulcerative colitis (UC) are considered inadequate owing to certain limitations. There have been reports on the anti-inflammatory effects of 2'-hydroxycinnamaldehyde (HCA). However, whether HCA can improve UC is still unclear. Here, we aimed to investigate the pharmacological effects of HCA on UC and its underlying molecular mechanisms.
methodsThe pharmacological effects of HCA were comprehensively investigated in 2 experimental setups: mice with dextran sulfate sodium (DSS)-induced colitis and lipopolysaccharide (LPS)-treated fetal human colon (FHC) cells. Furthermore, the interaction between HCA and signal transducer and activator of transcription 3 (STAT3) was investigated using molecular docking. The FHC cells with STAT3 knockdown or overexpression and mice with intestinal epithelium-specific STAT3 deletion (STAT3ΔIEC) were used to evaluate whether STAT3 mediated the pharmacological effects of HCA.
results2'-Hydroxycinnamaldehyde attenuated dysregulated expression of inflammatory cytokines in a dose-dependent manner while increasing the expression of tight junction proteins, reducing the apoptosis of intestinal epithelial cells, and effectively alleviating inflammation both in vivo and in vitro. 2'-Hydroxycinnamaldehyde bound directly to STAT3 and inhibited its activation. The modulation of STAT3 activation levels due to STAT3 knockdown or overexpression influenced the mitigating effects of HCA on colitis. Further analysis indicated that the remission effect of HCA was not observed in STAT3ΔIEC mice, indicating that STAT3 mediated the anti-inflammatory effects of HCA.
conclusionsWe present a novel finding that HCA reduces colitis severity by attenuating intestinal mucosal barrier damage via STAT3. This discovery holds promise as a potential new strategy to alleviate UC.
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