Phytomedicine : international journal of phytotherapy and phytopharmacology · 2025
Parishin from Gastrodia elata ameliorates DSS induced colitis and anxiety-like behavior in mice by regulating intestinal barrier function and microviota-gut-brain axis.
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Liu Xiaoxue, Zhou Hejiang, Yang Na, Yang Lu-Jun, Zi Zheng-Ying, Han Ya-Lan, He Jinsong, Su Ling-Yan
Аннотация
BACKGROUND: Inflammatory bowel diseases (IBDs), including colitis, are commonly associated with dysfunctional intestinal barriers and dysregulated gut microbiota. Moreover, current medications for IBD cause serious side effects with prolonged use. Parishin, a phenolic glucoside isolated from Gastrodia elata, is known for its medicinal value in anti-aging properties. However, the therapeutic effects of Parishin on colitis and the underlying mechanisms remain largely unexplored.
PURPOSE: The aim of this study was to examine the protective effects of Parishin on colitis and related anxiety mood disorder in mice, as well as to explore its potential mechanisms.
METHODS: This study employed a DSS-induced colitis mouse model to evaluate Parishin's therapeutic effects. Mice were divided into control, model, and Parishin treatment groups, followed by DAI, histopathology, inflammatory cytokines, gut barrier proteins, gene expression, behavioral changes, and gut microbiota composition.
RESULTS: We demonstrated that Parishin alleviated symptoms such as weight loss, a colon shortening, and a high disease activity index in a dextran sulfate sodium (DSS)-induced colitis mouse model. Parishin strengthened the intestinal barrier by increasing the expression of tight junction proteins and mucin. Furthermore, Parishin significantly reduced the production of pro-inflammatory cytokines in the serum, colon and spleen of mice with DSS. Notably, Parishin treatment attenuated DSS-induced anxiety-like behavior by activating GABA receptors and regulating the FKBP5 level. Gut microbiota analysis showed that Parishin restored the DSS-disturbed microbiota of the mice.
CONCLUSION: These findings demonstrate that Parishin may attenuate DSS-induced colitis and anxiety-like behavior by enhancing the intestinal barrier and regulating the gut microbiota, supporting the development of a Parishin-based strategy for IBD prevention or treatment.
PURPOSE: The aim of this study was to examine the protective effects of Parishin on colitis and related anxiety mood disorder in mice, as well as to explore its potential mechanisms.
METHODS: This study employed a DSS-induced colitis mouse model to evaluate Parishin's therapeutic effects. Mice were divided into control, model, and Parishin treatment groups, followed by DAI, histopathology, inflammatory cytokines, gut barrier proteins, gene expression, behavioral changes, and gut microbiota composition.
RESULTS: We demonstrated that Parishin alleviated symptoms such as weight loss, a colon shortening, and a high disease activity index in a dextran sulfate sodium (DSS)-induced colitis mouse model. Parishin strengthened the intestinal barrier by increasing the expression of tight junction proteins and mucin. Furthermore, Parishin significantly reduced the production of pro-inflammatory cytokines in the serum, colon and spleen of mice with DSS. Notably, Parishin treatment attenuated DSS-induced anxiety-like behavior by activating GABA receptors and regulating the FKBP5 level. Gut microbiota analysis showed that Parishin restored the DSS-disturbed microbiota of the mice.
CONCLUSION: These findings demonstrate that Parishin may attenuate DSS-induced colitis and anxiety-like behavior by enhancing the intestinal barrier and regulating the gut microbiota, supporting the development of a Parishin-based strategy for IBD prevention or treatment.