The biotransforamtion of swertiamarin has been carried out using Aspergillus niger. The results showed that 60% swertiamarin were metabolized into two metabolites during the 5 days of biotransformation. The metabolites were identified as erythrocentaurin and 5-ethylidene-8-hydroxy-3,4,5,6,7,8-hexahydro-1Hpyrano[3,4-c]-pyridine-1-one, a novel alkaloid, with NMR and MS. The hydrolysis of glucosidic bond catalyzed by β-D-glucosidase was found to be the rate-limiting reaction in pathway of biotransformation of swertiamarin.
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Article Synopsis
- The study focuses on how swertiamarin (SWE) influences macrophages in the tumor microenvironment to adopt an M1 phenotype, which helps in fighting tumors.
- SWE leads to an increase in M1 macrophages and CD86+ cells by activating the STING-NF-κB signaling pathway, but these effects diminish when STING or P65 are knocked out.
- In animal experiments, SWE was found to reduce tumor growth and boost M1 macrophage formation through the STING-NF-κB pathway, underlining its potential as an anti-tumor agent.
[Swertiamarin ameliorates 2, 4, 6-trinitrobenzenesulfonic acid-induced colitis in mice by inhibiting intestinal epithelial cell apoptosis].
Nan Fang Yi Ke Da Xue Xue Bao
August 2024
Department of Radiology, First Affiliated Hospital of Anhui Medical University, Hefei 230000, China.
Objective: To investigate the mechanism by which swertiamarin (STM) ameliorates CD-like colitis in mice.
Methods: A Caco-2 cell model of TNF--stimulated apoptosis was established and divided into three groups: Con, TNF- and STM, and the effects of STM on apoptosis and barrier function were assessed by Tunel staining, western blotting, immunofluorescence, and transepithelial electric resistance (TEER). A mouse model of 2, 4, 6-trinitrobenzenesulfonic acid (TNBS) -induced CD-like colitis was established to assess the effects of STM on colitis, intestinal barrier function and epithelial cell apoptosis.
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