ArticleFood science & nutrition2026
Chlorogenic Acid Ameliorate Lipopolysaccharide Induced Intestinal Acute Inflammatory Injury via Inhibiting Cytokines Production and Activating Intestinal Stem Cells.
Article in Food science & nutrition, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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
1 citing paper in PubMed.
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Several studies have confirmed that chlorogenic acid (CGA) has beneficial effects on intestinal health. This study aimed to investigate the protective effect and underlying mechanism of CGA in lipopolysaccharide (LPS)-induced intestinal injured mice. Histological analysis of duodenal epithelial morphology and tight junction-related gene expression indicated that CGA helps preserve intestinal barrier integrity. Quantitative PCR analysis showed that CGA suppressed the expression of pro-inflammatory factors including interferon-γ (Ifn-γ), interleukin-7 (Il-7), tumor necrosis factor-α (Tnf-α), and upregulated the anti-inflammatory cytokines interleukin-10 (Il-10) in LPS-induced enteritis mice. Furthermore, compared to LPS-treatment mice, CGA supplementation sustained intestinal stem cell (ISCs) activity, including proliferation and differentiation. Additionally, CGA inhibited LPS-induced activation of the Janus kinase/signal transducers and activators of transcription (JAK/STAT) pathway, as evidenced by a reduction in the expression of Jak2, Jak3, and Stat1. This effect was comparable to that of Tofacitinib, a known JAK/STAT pathway inhibitor. Collectively, these findings suggest that CGA protects intestinal epithelial integrity and alleviates intestinal injury by suppressing inflammatory responses and preserving ISC activity via inhibition of the JAK/STAT signaling pathway.
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