Title:Ginsenoside Rb1 Suppresses AOM/DSS-induced Colon Carcinogenesis
Volume: 23
Issue: 9
Author(s): Ling Wang, Qing-Qing Zhang, Yu-Yu Xu, Rui Zhang, Qing Zhao, Yu-Qing Zhang, Xue-Hong Huang, Bin Jiang*Min Ni*
Affiliation:
- Colorectal Disease Center, Nanjing Hospital of
Chinese Medicine Affiliated to Nanjing University of Chinese Medicine, Nanjing University of Chinese Medicine, Nanjing, 210022,
China
- Colorectal Disease Center, Nanjing Hospital of
Chinese Medicine Affiliated to Nanjing University of Chinese Medicine, Nanjing University of Chinese Medicine, Nanjing, 210022,
China
Keywords:
Colorectal cancer, ginsenoside Rb1, inflammation, gut microenvironment, colitis, carcinogenesis.
Abstract:
Background: Colorectal cancer (CRC) is the third most common cancer worldwide. Current treatments, including
surgery, radiotherapy, and chemotherapy, are limited by severe side effects and the development of resistance.
Objective: Therefore, it is important to find additional therapies to combat the problem. Ginsenoside Rb1 is the main
active ingredient of ginseng, which is a well-known herb in traditional Chinese medicine. Ginsenoside is reported to
play an important role in the prevention and treatment of cancer.
Methods: We established Azoxymethane (AOM)/Dextran sodium sulfate (DSS) colon cancer model based on inflammation,
observed the beneficial effect of ginsenoside Rb1, and detected the changes in gut microbiota.
Results: Our experimental results showed that ginsenoside Rb1 significantly reduced the levels of TNF-α, IL-6, IL-
17A, IL-33, IL-1β, and IL-22, increased the level of IL-10, and also changed the gut microbiota composition. These
results suggested that ginsenoside Rb1 can be used to prevent inflammation-associated CRC development and may
provide an effective therapeutic strategy for CRC by relieving chronic inflammation and restoring the gut microenvironment
in the AOM/DSS-induced model of colitis-associated colorectal cancer in mice.
Conclusion: Ginsenoside Rb1 significantly attenuated AOM/DSS-induced colon carcinogenesis.