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Ginsenoside Rb1 Alleviates DSS-Induced Ulcerative Colitis by Protecting the Intestinal Barrier Through the Signal Network of VDR, PPARγ and NF-κB. | LitMetric

AI Article Synopsis

  • Ginseng, particularly its component Ginsenoside Rb1 (GRb1), shows promise in treating ulcerative colitis (UC) by reducing intestinal inflammation and improving the integrity of the intestinal barrier.
  • In laboratory studies on mice with UC, GRb1 treatment led to lower levels of pro-inflammatory cytokines and higher levels of anti-inflammatory cytokines, positively affecting intestinal health.
  • The research suggests that GRb1's beneficial effects are linked to its interaction with specific signaling pathways (VDR, PPARγ, and NF-κB) that regulate inflammation and barrier function in the intestines.

Article Abstract

Purpose: Ginseng ( Meyer) is an herbal medicine used in traditional Chinese medicine (TCM), has the effects of treating colitis and other diseases. Ginsenoside Rb1 (GRb1), a major component of ginseng, modulates autoimmunity and metabolism. However, the mechanism underlying GRb1 treatment of ulcerative colitis (UC) has not yet been elucidated. UC is a refractory inflammatory bowel disease (IBD) with a high recurrence rate, and researches on new drugs for UC have been in the spotlight for a long time.

Methods: Mice with DSS-induced UC were treated with GRb1 or 0.9% saline for 10 days. Colon tissue of UC mice was collected to detect the levels of intestinal inflammatory cytokines and integrity of the intestinal barrier. RNA-seq and network pharmacology were used to predict the therapeutic targets of GRb1 during UC treatment.

Results: GRb1 treatment alleviated intestinal inflammation and improved intestinal barrier dysfunction in UC mice. Specifically, GRb1 downregulated the levels of pro-inflammatory cytokines such as TNF-α and IL-6, while upregulating the level of the anti-inflammatory cytokine IL-10. Additionally, GRb1 treatment increased the levels of tight junction proteins including ZO-1, Occludin, and E-cadherin, which are crucial for maintaining intestinal barrier integrity. Further analyses using RNA-seq and network pharmacology suggested that these effects might involve the regulation of GRb1 in the signal transduction network of VDR, PPARγ, and NF-κB.

Conclusion: The study demonstrated that GRb1 effectively alleviated UC by modulating intestinal inflammation and protecting the integrity of the intestinal barrier through the signal transduction network of VDR, PPARγ, and NF-κB.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11531243PMC
http://dx.doi.org/10.2147/DDDT.S481769DOI Listing

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