ArticleMolecular biology reports2025
Chlorogenic acid reduces Lipopolysaccharide-Induced intestinal inflammation through Inhibition of acetylcholinesterase and activation of muscarinic receptors.
Article in Molecular biology reports, 2025. 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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1 citing paper in PubMed.
- Assessing theAntioxidants (Basel, Switzerland) · 2026Article
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4 authors.
Funding
Abstract
backgroundChlorogenic acid (CGA) is a dietary polyphenol with well-documented anti-inflammatory property. However, its effects on cholinergic signaling during inflammation remain under-explored.
aimTo investigate the role of CGA in modulating lipopolysaccharide (LPS) induced inflammation and epithelial barrier dysfunction in human intestinal cells, with a focus on cholinergic pathways involving acetylcholinesterase (AChE) and muscarinic receptors.
methodsCaco-2 cell monolayers were treated with LPS, with or without CGA. Inflammatory markers, tight junction proteins, mucin secretion, and cholinergic gene expression were assessed via qRT-PCR, ELISA, immunofluorescence, and Alcian Blue staining. AChE activity was measured in cell supernatants. Kinetic studies were done with pure human and electric eel enzymes. Inhibition kinetics and molecular docking was performed. Darifenacin was used to probe the role of muscarinic receptors.
resultsCGA significantly suppressed LPS-induced expression of TNF-α, IL-6, and COX-2, and restored tight junction protein expression (ZO-1, occludin) and sucrase-isomaltase mRNA levels. CGA attenuated LPS-induced mucin hypersecretion without affecting MUC2 gene or protein expression. It also reversed LPS-induced upregulation of α7 nicotinic ACh receptors and further elevated choline acetyltransferase (ChAT) and M3 muscarinic receptor (mAChR3) expression. These effects were abolished by muscarinic receptor antagonism, indicating CGA's dependence on mAChR signaling. CGA reduced cholinesterase activity in supernatants. Kinetic studies revealed that CGA competitively inhibited HuAChE (IC₅₀ = 225 nM; K
conclusionsCGA protects intestinal epithelial cells from inflammatory damage by enhancing cholinergic anti-inflammatory signaling through specific AChE inhibition and regulation. Future studies should validate these effects in vivo and confirm functional receptor activation and bioavailability.
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