There are abundant sources of anticancer drugs in nature that have a broad prospect in anticancer drug discovery. Natural compounds, with biological activities extracted from plants and marine and microbial metabolites, have significant antitumor effects, but their mechanisms are various. In addition to providing energy to cells, mitochondria are involved in processes, such as cell differentiation, cell signaling, and cell apoptosis, and they have the ability to regulate cell growth and cell cycle. Summing up recent data on how natural products regulate mitochondria is valuable for the development of anticancer drugs. This review focuses on natural products that have shown antitumor effects via regulating mitochondria. The search was done in PubMed, Web of Science, and Google Scholar databases, over a 5-year period, between 2015 and 2020, with a keyword search that focused on natural products, natural compounds, phytomedicine, Chinese medicine, antitumor, and mitochondria. Many natural products have been studied to have antitumor effects on different cells and can be further processed into useful drugs to treat cancer. In the process of searching for valuable new drugs, natural products such as terpenoids, flavonoids, saponins, alkaloids, coumarins, and quinones cover the broad space.

Background/Objectives: Danggui Beimu Kushen pill (DBK) is a traditional Chinese medicine renowned for its efficacy in the treatment of inflammatory conditions. It has been used in the modern clinical treatment of ulcerative colitis (UC). Further research is required to clarify its underlying mechanisms. Methods: DBK compounds were analyzed using UPLC-ESI-MS/MS. A mouse model of Dextran sulfate sodium (DSS)-induced UC was used to assess the efficacy of DBK. Network pharmacology identified DBK targets in UC, which were validated by molecular docking simulations. Cytokine levels were quantified using ELISA. Western blotting, immunofluorescence (IF), and immunohistochemistry (IHC) were employed to explore its underlying molecular mechanisms. Results: DBK treatment enhanced body weight and colon length in mice with DSS-induced colitis. Inflammatory cytokine levels (TNF-α, IL-1β, IL-6, IL-23, and IL-17A) were notably decreased in both serum and colon tissues. Network pharmacology and molecular docking analyses identified the IL-6/IL-6R and IL-17A/IL-17RA signaling pathways as crucial for the DBK treatment of UC. Additional validation using WB, IHC, and IF analyses demonstrated that DBK alleviated UC by suppressing the IL-6/STAT3 and IL-17/TRAF6/NF-κB pathways. Conclusions: DBK mitigates intestinal injury in mice with DSS-induced colitis and exerts therapeutic effects on UC by inhibiting the IL-6/IL-6R and IL-17A/IL-17RA signaling pathways to reduce inflammation. These findings provide significant insights into the mechanism of DBK treatment for UC.