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Study Design

Type
Clinical Trial
Population
Mice with DSS-induced colitis
Methods
In vivo experiment with mice.
  • Animal Study

Abstract

Cordyceps exopolysaccharide (CEP) has shown emerging potential in adjustment of gut microbiota and immune cell function. In this study, a water-soluble CEP with a molecular weight of 58.14 kDa was extracted from the fermentation broth of Paecilomyces hepiali, an endophytic fungus of Cordyceps sinensis. Our results indicated that Paecilomyces hepiali polysaccharide (PHP) showed significantly preventive potential on dextran sulfate sodium (DSS)-induced colitis in mice, which can prevent colon shortening, reduce intestinal epithelial cell (IEC) destruction, suppress inflammatory cell infiltration, and regulate the balance between regulatory T (Treg) cells and T helper type 17 (Th17) cells. Meanwhile, the disturbed gut microbiota was partially restored after PHP treatment. Further Pearson correlation coefficient analyses exhibited that the alteration of the gut microbiota was significantly related to adjustment of the IEC barrier and Treg/Th17 balance. In conclusion, all findings proposed that purified PHP has the potential to develop into a promising agent for colitis prevention and adjuvant therapy via maintaining intestinal homeostasis of gut microbiota and immune system.

Keywords: Paecilomyces hepialid; cordyceps polysaccharide; gut microbiota; intestinal homeostasis; ulcerative colitis.

Research Insights

SupplementDoseHealth OutcomeEffect TypeEffect SizeSource
Paecilomyces hepialiImproved Gut Microbiota BalanceBeneficial
Moderate
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Meanwhile, the disturbed gut microbiota was partially restored after PHP treatment.

Paecilomyces hepialiImproved Immune BalanceBeneficial
Moderate
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regulate the balance between regulatory T (Treg) cells and T helper type 17 (Th17) cells

Paecilomyces hepialiReduced Colitis SeverityBeneficial
Moderate
View source

PHP showed significantly preventive potential on dextran sulfate sodium (DSS)-induced colitis in mice, which can prevent colon shortening, reduce intestinal epithelial cell (IEC) destruction, suppress inflammatory cell infiltration

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