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Sea Buckthorn Polysaccharide Ameliorates Colitis.

Qinqin Ouyang1, Xin Li2, Yongheng Liang1

  • 1College of Life Sciences, Nanjing Agricultural University, Nanjing 210000, China.

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|May 11, 2024
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Summary

Sea buckthorn polysaccharide (SBP) pretreatment alleviates ulcerative colitis (UC) by reducing inflammation and gut barrier damage. SBP modulates gut microbiota, increasing beneficial bacteria and short-chain fatty acids (SCFAs) for colitis relief.

Keywords:
SCFAsgut microbiotainflammationinflammatory bowel diseasesea buckthorn polysaccharide

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Area of Science:

  • Gastroenterology
  • Microbiology
  • Immunology

Background:

  • Ulcerative colitis (UC) involves chronic intestinal inflammation and ulceration.
  • Sea buckthorn polysaccharide (SBP) is a bioactive compound from sea buckthorn berries with potential therapeutic benefits.
  • The exact mechanisms of SBP's action in UC are not fully understood.

Purpose of the Study:

  • To investigate the effects of SBP pretreatment on dextran sulfate sodium (DSS)-induced colitis.
  • To explore the role of SBP-modulated gut microbiota in ameliorating colitis.

Main Methods:

  • Induction of colitis in mice using DSS.
  • Pretreatment of mice with SBP.
  • Fecal microbiota transplantation (FMT) from SBP-treated mice to DSS-treated mice.
  • Assessment of inflammation, oxidative stress, intestinal barrier integrity, gut microbiota composition, and short-chain fatty acid (SCFA) production.

Main Results:

  • SBP pretreatment significantly reduced inflammation, oxidative stress, and intestinal barrier damage in DSS-induced colitis.
  • Microbiota from SBP-treated mice conferred anti-inflammatory and antioxidant effects.
  • SBP-modulated microbiota improved colonic barrier integrity, increased beneficial bacteria, and enhanced SCFA production.

Conclusions:

  • SBP ameliorates colitis by modulating the gut microbiota.
  • SBP promotes SCFA-producing bacteria, leading to increased SCFA levels.
  • Pre-emptive SBP supplementation shows promise for managing colitis through gut microbiota regulation.