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Ginsenoside Rk3 Ameliorates Obesity-Induced Colitis by Modulating Lipid Metabolism in C57BL/6 Mice
Weimin Wang1, Hongwei Chen2, Wenyuan Zhang3
1College of Food Science and Nutritional Engineering, China Agricultural University, Beijing 100083, China.
Abstract:
Lipid metabolism is closely related to obesity and its complications. Our previous study found that ginsenoside Rk3 (Rk3), a natural bioactive substance derived from ginseng, can effectively alleviate obesity-induced colitis, while its impact on the improvement of the lipid metabolism disorder remains unclear. Here, we demonstrated that Rk3 significantly alleviated inflammation, oxidative stress, and lipid dysregulation in high-fat diet-induced colitis C57BL/6 mice. The potential mechanism by which Rk3 mitigated colon inflammation in the context of obesity may involve the modulation of polyunsaturated fatty acid metabolism with specific attention to n-6 fatty acids, linoleic acid, and arachidonic acid. Rk3 intervention markedly reduced the production of pro-inflammatory factors (PGE2, PGD2, TXB2, HETE, and HODE) by inhibiting cyclooxygenase and lipoxygenase pathways, while enhancing the production of anti-inflammatory factors (EET and diHOME) via cytochrome P450 pathways. Our findings suggest that Rk3 is a potential anti-inflammatory natural drug that can improve obesity-induced intestinal inflammation by regulating lipid metabolism.
Insights
Ginsenoside Rk3 (Rk3) effectively reduces obesity-related gut inflammation and improves lipid metabolism by altering fatty acid pathways. This natural compound shows potential as an anti-inflammatory drug for metabolic disorders.
Area of Science:
- Biochemistry
- Pharmacology
- Gastroenterology
Background:
- Lipid metabolism is linked to obesity and its complications.
- Ginsenoside Rk3 (Rk3) previously showed efficacy against obesity-induced colitis.
- The effect of Rk3 on lipid metabolism disorders was previously unclear.
Purpose of the Study:
- To investigate the impact of Rk3 on lipid metabolism disorders in obesity-induced colitis.
- To elucidate the mechanism by which Rk3 mitigates colon inflammation in obese mice.
Main Methods:
- High-fat diet-induced colitis model in C57BL/6 mice.
- Assessment of inflammation, oxidative stress, and lipid dysregulation.
- Analysis of polyunsaturated fatty acid metabolism, including n-6 fatty acids (linoleic acid, arachidonic acid).
- Measurement of pro-inflammatory and anti-inflammatory lipid mediators via cyclooxygenase, lipoxygenase, and cytochrome P450 pathways.
Main Results:
- Rk3 significantly alleviated inflammation, oxidative stress, and lipid dysregulation.
- Rk3 modulated polyunsaturated fatty acid metabolism, particularly n-6 fatty acids.
- Rk3 reduced pro-inflammatory factors (PGE2, PGD2, TXB2, HETE, HODE) by inhibiting COX/LOX pathways.
- Rk3 enhanced anti-inflammatory factors (EET, diHOME) via CYP450 pathways.
Conclusions:
- Rk3 improves obesity-induced intestinal inflammation by regulating lipid metabolism.
- Rk3 demonstrates potential as a natural anti-inflammatory drug for metabolic disorders.
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