期刊
MOLECULES
卷 27, 期 3, 页码 -出版社
MDPI
DOI: 10.3390/molecules27030628
关键词
ginsenosides; Rh2; cancer therapy; ROS; Nrf2; reporter assay; computer modeling
资金
- Ministry of Science and Higher Education of the Russian Federation [075-02-2020-1584]
- Far Eastern Federal University [075-02-2020-1584]
- Russian Foundation for Basic Research [17-04-01480a, 20-04-00943, 20 04-00921]
Ginsenoside Rh2 enhances the efficacy of doxorubicin treatment in murine models of solid and ascites Ehrlich's adenocarcinoma by suppressing tumor cell adhesion and invasion. Rh2 also reduces the toxicity of doxorubicin towards non-cancerous cells by activating the Nrf2-driven antioxidant program.
Ginsenoside Rh2 increases the efficacy of doxorubicin (DOX) treatment in murine models of solid and ascites Ehrlich's adenocarcinoma. In a solid tumor model (treatment commencing 7 days after inoculation), DOX + Rh2 co-treatment was significantly more efficacious than DOX alone. If treatment was started 24 h after inoculation, the inhibition of tumor growth of a solid tumor for the DOX + Rh2 co-treatment group was complete. Furthermore, survival in the ascites model was dramatically higher for the DOX + Rh2 co-treatment group than for DOX alone. Mechanisms underlying the combined DOX and Rh2 effects were studied in primary Ehrlich's adenocarcinoma-derived cells and healthy mice's splenocytes. Despite the previously established Rh2 pro-oxidant activity, DOX + Rh2 co-treatment revealed no increase in ROS compared to DOX treatment alone. However, DOX + Rh2 treatment was more effective in suppressing Ehrlich adenocarcinoma cell adhesion than either treatment alone. We hypothesize that the benefits of DOX + Rh2 combination treatment are due to the suppression of tumor cell attachment/invasion that might be effective in preventing metastatic spread of tumor cells. Ginsenoside Rh2 was found to be a modest activator in a Neh2-luc reporter assay, suggesting that Rh2 can activate the Nrf2-driven antioxidant program. Rh2-induced direct activation of Nrf2 might provide additional benefits by minimizing DOX toxicity towards non-cancerous cells.
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