# UPLC-Q-TOF-MS/MS and Network Pharmacology Approaches to Explore the Active Compounds and Mechanisms of Kadsura coccinea for Treating Rheumatoid Arthritis

## TL;DR

This study identifies compounds in Kadsura coccinea that may help treat rheumatoid arthritis by targeting inflammation and immune pathways.

## Contribution

The study combines chemical profiling and network pharmacology to reveal multi-target mechanisms of Kadsura coccinea in rheumatoid arthritis.

## Key findings

- 90 compounds were identified, including 36 lignans and 29 triterpenoids from Kadsura coccine.
- Key compounds like kadcoccinone F and schisantherin M bind to RA-related targets such as MMPs and JAKs.
- Molecular docking confirmed strong interactions between KC compounds and inflammatory targets.

## Abstract

This study aimed to systematically identify the active constituents of Kadsura coccinea (Lem.) A. C. Smith (KC) and elucidate their potential mechanisms in treating rheumatoid arthritis (RA) using an integrated analytical and computational approach. Chemical profiling of KC root extract was performed by UPLC-Q-TOF-MS/MS. Active compounds and their targets were predicted using the SwissTargetPrediction database, while RA-related genes were retrieved from OMIM, GeneCards, and DisGeNET. A compound–target network was constructed and analyzed via Cytoscape. Functional enrichment analyses and protein–protein interaction (PPI) clustering were conducted to identify key pathways. Molecular docking was employed to validate interactions between core compounds and key RA targets. A total of 90 compounds were identified, primarily 36 lignans and 29 triterpenoids. Network analysis revealed 145 overlapping targets between KC and RA. These targets were further associated with 65 compounds derived from KC. Key compounds such as kadcoccinone F, kadsuralignan I and schisantherin M were linked to hub targets including MAPK14, MMPs, and JAKs, which are involved in inflammatory signaling, matrix degradation, and immune regulation. Molecular docking confirmed strong binding affinities (ΔG < −5.0 kcal/mol) between representative KC compounds and targets like MMP1, MMP2, JAK2 and JAK3, supported by analyses of hydrogen bonding, hydrophobic, and π-interactions. These results suggest that KC exerts anti-RA effects through multi-component, multi-target mechanisms, primarily modulating inflammatory signaling, immune cell recruitment, and tissue-destructive pathways. This study provides a pharmacological basis for the traditional use of KC in RA management and supports its potential as a complementary therapeutic agent.