Ginsenoside Rk3 Ameliorates Obesity-Induced Colitis by Regulating of Intestinal Flora and the TLR4/NF-κB Signaling Pathway in C57BL/6 Mice.

Abstract

Obesity-induced colonic inflammation-stimulated colitis is one of the main causes of colorectal cancer. Dietary phytochemicals are considered to be an effective strategy for relieving obesity-induced inflammatory diseases such as diabetes and colitis. Ginsenoside Rk3 (Rk3) is the main bioactive component of ginseng. Our previous study has demonstrated that Rk3 can effectively alleviate obesity-induced type 2 diabetes, but whether it plays a beneficial role in obesity-induced colitis remains poorly understood. Here, we found that Rk3 intervention repaired the intestinal barrier dysfunction by increasing the expression of the tight junction proteins (zonula occludens-1, claudin, and occludin), and reduced colonic inflammatory cytokine levels, oxidative stress, and macrophage infiltration in high-fat diet-induced mice. Importantly, Rk3 effectively ameliorated the metabolic dysbiosis of intestinal flora with significantly decreased Firmicute/Bacteroidete ratios and suppressed the inflammatory cascade by inhibiting the TLR4/NF-κB signaling pathway. Taken together, our findings indicate that Rk3 can be used as a potential natural anti-inflammatory agent to reduce chronic obesity-induced colitis.

• Authors: Hongwei Chen, Haixia Yang, Jianjun Deng, Daidi Fan
• Journal: Journal of agricultural and food chemistry (J Agric Food Chem) Vol. 69 Issue 10 Pg. 3082-3093 (Mar 17 2021) ISSN: 1520-5118 [Electronic] United States
• PMID: 33621094 (Publication Type: Journal Article)

Chemical References

• Ginsenosides
• NF-kappa B
• Tlr4 protein, mouse
• Toll-Like Receptor 4
• ginsenoside Rk3

Topics

• Animals
• Colitis (drug therapy, genetics)
• Diabetes Mellitus, Type 2
• Gastrointestinal Microbiome
• Ginsenosides
• Mice
• Mice, Inbred C57BL
• NF-kappa B (genetics, metabolism)
• Obesity (drug therapy)
• Signal Transduction
• Toll-Like Receptor 4 (genetics)