# Rice-Fried and Sun-Dried Ginseng: A Comparative Study of Chemical Composition and Protective Effects Against Ulcerative Colitis

## TL;DR

This study compares rice-fried and sun-dried ginseng to see how their chemical differences affect their ability to protect against ulcerative colitis.

## Contribution

The study reveals that rice-frying ginseng enhances its anti-inflammatory and protective effects against ulcerative colitis through chemical composition changes.

## Key findings

- Rice-fried ginseng (RFG) showed improved anti-inflammatory effects and protective actions in ulcerative colitis models compared to sun-dried ginseng.
- RFG altered gut microbiota and lipid metabolism, and reduced phosphorylation of key inflammatory signaling proteins like PI3K, Akt, and NF-κB.
- RFG increased cell viability and tight junction proteins in Caco-2 cells and improved colon health in mice.

## Abstract

Ginseng (Panax ginseng C. A. Mey.), a traditional Chinese medicine, exhibits spleen-fortifying, anti-inflammatory, and anti-ulcerative colitis (UC) effects. Rice-fried ginseng (RFG), prepared by stir-frying with rice together, yields a marked enrichment of rare ginsenosides, which is hypothesized to enhance its anti-inflammatory and anti-UC effects. Therefore, in this study, the chemical compositions of RFG and sun-dried ginseng (SDG) were systematically compared using LC–MS combined with MS-DIAL, and their protective effects against UC were evaluated using lipopolysaccharide (LPS)-induced Caco-2 cells and a dextran sulfate sodium (DSS)-induced UC mouse model. Rice-frying markedly altered the chemical composition of ginseng, and a total of 64 major compounds were identified, of which 31 increased and 33 decreased after processing. These compositional changes were associated with enhanced anti-inflammatory and immunomodulatory effects of RFG. Consistently, RFG enhanced Caco-2 cell viability, decreased TNF-α, IL-1β, and IL-6, and increased ZO-1, occludin, claudin-1, and E-cadherin. In DSS-induced UC mice, RFG attenuated body weight loss, reduced DAI, increased colon length, and decreased the spleen index, accompanied by improved histopathology, reduced pro-inflammatory cytokine levels, and increased expression of tight-junction proteins (TJPs) in a dose-dependent manner. In addition, RFG ameliorated DSS-induced gut microbiota dysbiosis. Metabolomics and network pharmacology analyses highlighted disturbances in linoleic acid and arachidonic acid metabolism and emphasized the involvement of the PI3K–Akt and NF-κB signaling pathways. Western blotting demonstrated decreased phosphorylation of PI3K, Akt, IKKβ, and NF-κB after RFG intervention. Overall, compared with SDG, RFG showed stronger protective effects in vitro and in vivo, accompanied by improved inflammatory readouts, altered lipid-related metabolites and gut microbiota profiles, and reduced phosphorylation of PI3K, Akt, IKKβ, and NF-κB.