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Modern pharmacological studies have confirmed that ginsenosides are the main bioactive components of ginseng, and they are renowned for their good safety and wide application in food and dietary supplements. Preclinical studies have demonstrated that ginsenosides possess powerful antioxidant, anti-inflammatory, and anti-apoptotic properties, providing a mechanistic basis for their role in cancer prevention. Although early clinical trials showed promise in alleviating the side effects of chemotherapy, rigorous clinical research is still needed to determine its efficacy in cancer treatment. This review systematically explores the mechanism of interaction between ginsenoside classes and the intestinal microbiota in the hepatitis-driven carcinogenesis process from a nutritional perspective. The book elaborates on how specific ginsenosides, such as Rg3, compound K, and Rk1, exert different anti-cancer effects through various mechanisms. Additionally, the study also explores the dual role of the intestinal microbiota in the development of inflammation-related hepatocellular carcinoma. Pathogenic bacteria promote tumor occurrence through lipopolysaccharide (LPS)/Toll-like receptor 4 (TLR4)-driven inflammation and genotoxic bile acids (BA) metabolism, while beneficial microbiota exert protective effects by producing short-chain fatty acids and stabilizing the intestinal barrier. The key point is that it emphasizes the bidirectional interaction between ginsenosides and the intestinal microbiota: ginsenosides are metabolized by symbiotic bacteria into bioactive compounds, such as compound K, which then regulate the microbial composition and inhibit pro-inflammatory pathways. Through these findings, this review systematically clarifies the scientific basis for combining dietary ginsenosides with intestinal microbiota modulation for liver cancer prevention, while emphasizing the key bottlenecks in mechanism exploration and clinical translation. Future research must further elucidate the pharmacokinetic characteristics of active components, optimize delivery systems to enhance bioavailability, and conduct prospective multicenter human trials to verify long-term efficacy and safety. This mechanism framework not only provides theoretical support for the application of natural products in the prevention and control of chronic inflammation-related cancers, but also offers new insights into the development direction of personalized nutrition medicine.
Lv et al. (2026) studied this question.
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