Investigation of the Mechanism of Cinnamaldehyde in Irritable Bowel Syndrome Based via Network Pharmacology, Molecular Docking, and Animal Experiments.

Irritable bowel syndrome (IBS) is a prevalent functional gastrointestinal disorder characterized by abdominal pain and changes in bowel habits. Cinnamaldehyde (CA) possesses anti-inflammatory, antibacterial, and digestive-regulatory properties. However, its therapeutic potential for IBS and mechanisms are not understood. We employed network pharmacology to identify potential targets and pathways of CA against IBS. Core targets were validated through molecular docking, and further verified in an IBS rat model induced by neonatal maternal separation (NMS) and water avoidance stress (WAS). Network pharmacology identified 139 potential targets of CA related to IBS. Gene Ontology (GO) enrichment analysis highlighted key biological processes, cellular components, and molecular functions. Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis suggested involvement of pathways such as nitrogen metabolism, tyrosine metabolism, and cocaine addiction. A protein-protein interaction (PPI) network revealed 11 major targets, and molecular docking demonstrated strong binding affinities between CA and several targets, particularly MAOB, PARP1, HDAC1, JAK2, and MMP2. Animal experiments confirmed that CA significantly reduces MAOB, as well as TNF-α, IL-6, and IL-1β levels, thereby alleviating visceral hypersensitivity and anxiety and depression-like behaviors in IBS rats. These findings provide a scientific basis for developing CA as a potential natural therapeutic agent for IBS.