Ginsenoside Rk3 Ameliorates Obesity-Induced Colitis by Regulating of Intestinal Flora and the TLR4/NF-κB Signaling Pathway in C57BL/6 Mice.
Hongwei ChenHaixia YangJianjun DengDaidi FanPublished in: Journal of agricultural and food chemistry (2021)
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.
Keyphrases
- high fat diet induced
- insulin resistance
- oxidative stress
- type diabetes
- signaling pathway
- diabetic rats
- metabolic syndrome
- weight loss
- adipose tissue
- pi k akt
- weight gain
- toll like receptor
- drug induced
- inflammatory response
- induced apoptosis
- skeletal muscle
- glycemic control
- cardiovascular disease
- high glucose
- nuclear factor
- immune response
- randomized controlled trial
- dna damage
- lps induced
- poor prognosis
- ischemia reperfusion injury
- body mass index
- climate change
- endothelial cells
- mouse model
- physical activity
- risk assessment
- stress induced
- heat shock protein