ArticleNutrients2025
Anti-Inflammatory Effect of a Polysaccharide Derived from
Article in Nutrients, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed.
- Structural characterization, rheological properties, and skin bioactivities of a glucomannan from Bletilla striata.Natural products and bioprospecting · 2026Article
- Enzyme-AssistedInternational journal of molecular sciences · 2026Article
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
backgroundInflammation is a critical pathological process implicated in numerous diseases.
methodsIn this study, a water-soluble polysaccharide was extracted from the fruit pulp of
resultsJFP-Ps markedly diminished the production of nitric oxide (NO) and reactive oxygen species (ROS); reduced LPS-induced cell apoptosis by increasing glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) activity; and decreased pro-inflammatory cytokine levels, including interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α). JFP-Ps decreased inflammatory responses by inhibiting the production of gene and protein expression associated with the MAPK/ERK pathway. Additionally, metabolomic profiling revealed that LPS stimulation increased ether lipid metabolism while it decreased pantothenate and coenzyme A biosynthesis. These metabolic changes were partially reversed by JFP-Ps through inhibiting the synthesis of branched-chain amino acids.
conclusionsJFP-Ps may exert anti-inflammatory effects by concurrently modulating oxidative stress, inflammatory signaling, and metabolic reprogramming in macrophages.
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Registered trials
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