# Chlorogenic Acid Ameliorate Lipopolysaccharide Induced Intestinal Acute Inflammatory Injury via Inhibiting Cytokines Production and Activating Intestinal Stem Cells

## TL;DR

Chlorogenic acid protects the intestines from inflammation by reducing harmful immune responses and supporting stem cells.

## Contribution

This study reveals a new mechanism by which chlorogenic acid alleviates intestinal injury via JAK/STAT pathway inhibition and stem cell preservation.

## Key findings

- Chlorogenic acid preserves intestinal barrier integrity by maintaining tight junction gene expression.
- Chlorogenic acid suppresses pro-inflammatory cytokines and enhances anti-inflammatory cytokines in LPS-induced injury.
- Chlorogenic acid sustains intestinal stem cell activity and inhibits JAK/STAT pathway activation.

## 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.

This study aimed to investigate the protective effect and underlying mechanism of CGA in lipopolysaccharide (LPS)‐induced intestinal injury mice. The findings suggest that CGA alleviates intestinal injury by suppressing inflammatory response and preserving ISCs activity via inhibition of the JAK/STAT signaling pathway. All the results highlight that CGA has the potential to serve as a natural food compound for alleviating intestinal inflammation.