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The protective effect of betulinic acid against dextran sodium sulfate-induced ulcerative colitis in mice

Ming-Qi YANG 2, 2, 2,yu yang2, 2, 2,Jin-E YI   

  • Received:2024-01-10 Revised:2024-03-13 Online:2024-04-12 Published:2024-04-12
  • Contact: Jin-E YI

Abstract: Abstract: Objective To study the effect of betulinic acid (BA) on dextran sodium sulfate (DSS) -induced ulcerative colitis . Methods: Eighty-four C57BL / 6 mice were randomly divided into 7 groups, namely control group, BA group (0.5 mg / kg mb), DSS group, BA low, medium and high dose (0.25, 0.5, 1 mg / kg mb) + DSS groups, 5-aminosalicylic acid (5-aminosalicylic acid, 5-ASA) + DSS group. BA or 5-ASA was taken to the mice orally for 14 days; and on day 8th, 4% DSS solution was received for 7 days to induce colitis model. The length of the colon was measured, the pathological changes and ultrastructure were observed by hematoxylin and eosin (H & E) staining and transmission electron microscopy, the level of reactive oxygen species (ROS) was measured by immunofluorescence staining, and inflammatory factors were detected by real-time PCR and apoptosis was observed by TUNEL staining. Results: DSS induced colon length was significantly shortened (P<0.05), intestinal crypts were disordered with irregular surface, the number of goblet cells was reduced, intestinal tight junctions were incomplete, and microvilli were sparse. Meanwhile, exposure to DSS resulted in increased ROS levels and elevated inflammatory factors IL-1β, IL-6, and IL-10 (P<0.01), while decreasing TNF-α mRNA expression (P <0.01) in the colon, leading to cell apoptosis (P<0.01). However, pretreatment with either BA or 5-ASA reversed these phenomena, and the effect of BA was better than 5-ASA. Conclusion: BA has a preventive protective effect against DSS-induced colitis by improving the integrity of intestinal structure, reducing ROS production, improving the inflammatory response and inhibiting apoptosis.

Key words: Keywords: betulinic acid (BA), dextran sodium sulfate (DSS), colitis, reactive oxygen species (ROS), cell apoptosis

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