1. Palmatine ameliorates N-methyl-N'-nitrosoguanidine-induced chronic atrophic gastritis through the STAT1/CXCL10 axis.
- Author
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Zhou Y, Wang Q, Tang W, Ma Z, Yang Z, Li X, Chen W, Ma H, and Ye X
- Subjects
- Animals, Mice, Male, Signal Transduction drug effects, Mice, Inbred C57BL, Interleukin-17 metabolism, Tumor Necrosis Factor-alpha metabolism, Chronic Disease, STAT1 Transcription Factor metabolism, Gastritis, Atrophic drug therapy, Gastritis, Atrophic metabolism, Gastritis, Atrophic chemically induced, Methylnitronitrosoguanidine toxicity, Chemokine CXCL10 metabolism, Chemokine CXCL10 genetics, Berberine Alkaloids pharmacology
- Abstract
Chronic atrophic gastritis (CAG) is a prevalent preneoplastic condition of the stomach. Palmatine (PAL), an isoquinoline alkaloid isolated from Rhizoma Coptidis (RC), has significant anti-inflammatory properties and is often used to treat gastrointestinal disorders. However, the mechanism of PAL on CAG remains unclear. In this study, N-methyl-N'-nitrosoguanidine (MNNG) was used to induce CAG inflammatory disease models in vivo and in vitro. The efficacy of five alkaloids in RC and the dose-dependent effects of the most effective PAL in CAG mice were evaluated in two animal experiments. RNA-seq and western blot revealed that PAL significantly improved IL-17, TNF, and NF-kappa B inflammation-related signaling pathways. Further hub gene prediction and experimental validation revealed that PAL modulated the STAT1/CXCL10 axis, thereby exerting attenuation of CAG through the regulation of IL-17, TNF-α, and p-p65 expression. In conclusion, PAL was proposed to mitigate MNNG-induced CAG, potentially through the inhibition of oxidative stress and inflammatory responses via the STAT1/CXCL10 axis. This approach is an effective complement to the use of PAL in the treatment of CAG., (© 2024 Federation of American Societies for Experimental Biology.)
- Published
- 2024
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