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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.
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http://dx.doi.org/10.1016/j.phymed.2025.157019 | DOI Listing |
Arq Gastroenterol
September 2025
The Japanese Society of Internal Medicine, Editorial Department, Tokyo, Japan.
Background: This study aims to analyze research trends and emerging insights into gut microbiota studies from 2015 to 2024 through bibliometric analysis techniques. By examining bibliographic data from the Web of Science (WoS) Core Collection, it seeks to identify key research topics, evolving themes, and significant shifts in gut microbiota research. The study employs co-occurrence analysis, principal component analysis (PCA), and burst detection analysis to uncover latent patterns and the development trajectory of this rapidly expanding field.
View Article and Find Full Text PDFJ Crohns Colitis
September 2025
Department of Gastroenterology, University Hospital of Marseille Nord, Assistance Publique-Hôpitaux de Marseille (AP-HM), Aix-Marseille University, Marseille, France.
Background And Aims: While this strategy is frequently used for other biologics, real-world evidence on subcutaneous (SC) vedolizumab (VDZ) dose intensification in inflammatory bowel disease (IBD) is lacking. This study aimed to assess the effectiveness and safety of SC VDZ intensification.
Methods: We conducted a retrospective study in 25 centers including all patients with active ulcerative colitis (UC) or Crohn's disease (CD) (defined by PRO2), and incomplete or loss of response to SC VDZ 108mg EOW when the drug was intensified.
Anesthesiology
September 2025
Department of Anesthesiology, University of Florida College of Medicine, Gainesville, Florida.
Background: The brain-gut-microbiome (BGM) axis is a communication network through which the brain and gastrointestinal microbiota interact via neural, hormonal, immune, and gene expression mechanisms. Gut microbiota dysbiosis is thought to contribute to neurocognitive disorders, including perioperative neurocognitive disorder (PND), and to various metabolic abnormalities. Recently, we reported that sevoflurane induces neurocognitive deficits in exposed rats as well as their future offspring, with male offspring being particularly affected (intergenerational PND).
View Article and Find Full Text PDFInt J Surg
September 2025
Department of Cardiovascular Medicine, The Affiliated Panyu Central Hospital of Guangzhou Medical University (Cardiovascular Diseases Research Institute of Panyu District), Guangdong, China.
Curr Atheroscler Rep
September 2025
Division of Gastroenterology and Hepatology, Lynda K. and David M. Underwood Center for Digestive Health, Houston Methodist Hospital, Houston, TX, USA.
Purpose Of Review: This review aims to characterize the known cardiovascular (CV) manifestations associated with inflammatory bowel disease (IBD) and the underlying mechanisms driving these associations.
Recent Findings: Gut dysbiosis, a hallmark of patients with IBD, can result in both local and systemic inflammation, thereby potentially increasing the risk of cardiovascular disease (CVD) in the IBD population. Micronutrient deficiencies, anemia, and sarcopenia independently increase the risk of CVD and are frequent comorbidities of patients with IBD.