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Study on the Anti-Ulcerative Colitis Effect of Pseudo-Ginsenoside RT4 Based on Gut Microbiota, Pharmacokinetics, and
Hui Yu1, Caixia Wang1, Junzhe Wu1
1School of Pharmaceutical Sciences, Jilin University, Changchun 130021, China.
Abstract:
The purpose of this study was to explore the therapeutic effect of the oral administration of pseudo-ginsenoside RT4 (RT4) on ulcerative colitis (UC), and to determine the rate of absorption and distribution of RT4 in mice with UC. Balb/c mice were induced using dextran sulfate sodium salts (DSS) to establish the UC model, and 10, 20, or 40 mg/kg of RT4 was subsequently administered via gavage. The clinical symptoms, inflammatory response, intestinal barrier, content of total short-chain fatty acids (SCFAs), and gut microbiota were investigated. Caco-2 cells were induced to establish the epithelial barrier damage model using LPS, and an intervention was performed using 4, 8, and 16 µg/mL of RT4. The inflammatory factors, transient electrical resistance (TEER), and tight-junction protein expression were determined. Finally, pharmacokinetic and tissue distribution studies following the intragastric administration of RT4 in UC mice were performed. According to the results in mice, RT4 decreased the disease activity index (DAI) score, restored the colon length, reduced the levels of pro-inflammatory cytokines (TNF-α, IL-6, and IL-1β), and boosted the levels of immunosuppressive cytokine IL-10, increased the content of SCFAs, improved the colonic histopathology, maintained the ultrastructure of colonic mucosal epithelial cells, and corrected disturbances in the intestinal microbiota. Based on the results in caco-2 cells, RT4 reduced the levels of TNF-α, IL-6, and IL-1β; protected integrity of monolayers; and increased tight-junction protein expression. Additionally, the main pharmacokinetic parameters (Cmax, Tmax, t1/2, Vd, CL, AUC) were obtained, the absolute bioavailability was calculated as 18.90% ± 2.70%, and the main distribution tissues were the small intestine and colon. In conclusion, RT4, with the features of slow elimination and directional distribution, could alleviate UC by inhibiting inflammatory factors, repairing the intestinal mucosal barrier, boosting the dominant intestinal microflora, and modulating the expression of SCFAs.
Insights
Pseudo-ginsenoside RT4 (RT4) effectively treats ulcerative colitis (UC) by reducing inflammation and repairing the gut barrier. This study confirms RT4
Area of Science:
- Gastroenterology
- Pharmacology
- Microbiology
Background:
- Ulcerative colitis (UC) is a chronic inflammatory bowel disease with limited treatment options.
- Pseudo-ginsenoside RT4 (RT4) is a potential therapeutic agent for inflammatory conditions.
Purpose of the Study:
- To investigate the therapeutic effects of oral pseudo-ginsenoside RT4 (RT4) on ulcerative colitis (UC) in a mouse model.
- To determine the pharmacokinetic profile and tissue distribution of RT4 in UC mice.
Main Methods:
- Established UC model in Balb/c mice using dextran sulfate sodium salts (DSS).
- Administered RT4 orally at varying doses (10, 20, 40 mg/kg) and assessed clinical, inflammatory, barrier, SCFA, and microbiota parameters.
- Utilized Caco-2 cell models to evaluate RT4's effects on epithelial barrier integrity and inflammation.
- Conducted pharmacokinetic and tissue distribution studies of RT4 in UC mice.
Main Results:
- RT4 significantly reduced disease activity index (DAI) scores and restored colon length in UC mice.
- RT4 decreased pro-inflammatory cytokines (TNF-α, IL-6, IL-1β) and increased IL-10 levels, while boosting short-chain fatty acids (SCFAs) and improving gut microbiota.
- In vitro studies showed RT4 protected Caco-2 cell monolayers, reduced inflammatory factors, and increased tight-junction protein expression.
- Pharmacokinetic studies yielded an absolute bioavailability of 18.90% ± 2.70%, with primary distribution in the small intestine and colon.
Conclusions:
- Pseudo-ginsenoside RT4 (RT4) demonstrates significant therapeutic potential for ulcerative colitis (UC).
- RT4 alleviates UC by inhibiting inflammation, repairing the intestinal barrier, modulating gut microbiota, and influencing SCFA levels.
- RT4 exhibits favorable pharmacokinetic properties, including slow elimination and targeted distribution to the colon.
