# Exploring the Treatment of Cinnamomum Cassia Leaf Extract in Ulcerative Colitis: Network Pharmacology and In Vitro Investigations

## TL;DR

This study explores how cinnamomum cassia leaf extract may help treat ulcerative colitis by reducing inflammation and targeting key biological pathways.

## Contribution

The study identifies the anti-inflammatory mechanisms of cinnamomum cassia leaf extract in ulcerative colitis using network pharmacology and in vitro experiments.

## Key findings

- CCLE reduced nitric oxide and reactive oxygen species production in LPS-stimulated macrophages.
- CCLE inhibited macrophage migration and showed high binding affinity to key inflammatory targets.
- CCLE's effects are linked to pathways like PI3K-Akt, NF-κB, and TNF signaling.

## Abstract

Cinnamomum cassia essential oil production generates substantial waste, and the therapeutic potential of non-volatile constituents from cinnamomum cassia leaves in ulcerative colitis (UC) has not been fully explored. This research focused on identifying the principal components of cinnamomum cassia leaf extract (CCLE) through ultra-performance liquid chromatography quadrupole time-of-flight mass spectrometry (UPLC-QTOF-MS), and its anti-inflammatory potential was verified in vitro. A lipopolysaccharide (LPS)-stimulated RAW264.7 macrophage model was employed, with assessments performed through cell viability assays, Griess assay, fluorescent probe detection, wound healing, and Transwell migration assays. Network pharmacology analysis combined with molecular docking revealed that CCLE exerts therapeutic effects against UC by targeting key molecules including TNF, TLR4, STAT3, SRC, PTGS2, NFKB1, MMP9, EGFR, BCL2, and AKT1, with high binding affinity between these targets and CCLE components (especially Quercetin, Catechin, Naringenin, 3′,4′-dimethoxyflavonol, Procyanidin Bl, and Caffeic acid). Enrichment analysis indicated that the therapeutic effect of CCLE on UC was significantly associated with the PI3K-Akt signaling pathway, B cell receptor signaling pathway, NF-κB signaling pathway, TNF signaling pathway, and JAK-STAT signaling pathway. The experimental results demonstrated that CCLE markedly reduced the production of nitric oxide (NO) and reactive oxygen species (ROS) (* p < 0.05) and inhibited macrophage migration (* p < 0.05). In conclusion, CCLE appears to ameliorate UC via a multi-target regulatory mechanism involving inflammatory signaling pathways. These outcomes offer a scientific foundation for the further development of CCLE.