Dihydroartemisinin shift the immune response towards Th1, inhibit the tumor growth in vitro and in vivo
► DHA reduces tumor cell growth in RIN cell line, and also inhibits the growth of tumor tissue in vivo. ► Administration of DHA to tumor-bearing mice increases the level of IFN-γ and decreases the level of IL-4. ► Administration of DHA to tumor-bearing mice decreases the level of splenic CD4+CD25+ F...
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Veröffentlicht in: | Cellular immunology 2011, Vol.271 (1), p.67-72 |
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Sprache: | eng |
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Zusammenfassung: | ► DHA reduces tumor cell growth in RIN cell line, and also inhibits the growth of tumor tissue in vivo. ► Administration of DHA to tumor-bearing mice increases the level of IFN-γ and decreases the level of IL-4. ► Administration of DHA to tumor-bearing mice decreases the level of splenic CD4+CD25+ FOXP3+ regulatory T cells. ► By using an appropriate dose of DHA, new therapeutic aspects of this medicine in cancer therapy will be elucidated.
Some investigators have been found that Artemisinin and its derivates have inhibitory effect on growth of cancer cells. Among these derivatives, Dihydroartemisinin (DHA) is well known as a semi-synthetic one. In addition, T cells are proved to be essential for the destruction of cancer cells. In this research, we assessed the effects of DHA on tumor cell growth inhibition in vitro by MTT assay and in vivo by intra tumor injection of DHA against breast cancer. The results showed that the IC50 values of DHA for RIN pancreatic tumor cell line were 30μM and significant decrease in the tumor size in vivo. Also we evaluate the effect of DHA on the modulation of immune response in tumor bearing animals; these include the splenocyte proliferation using the BrdU kit; measurement of cytokine profile by ELISA, and evaluate the percentage of T regulatory cells in the spleen by flowcytometry. Our results demonstrated that a significant decrease in the level of IL-4 in the animals treated with DHA and significant decreased in the level of splenic CD4+CD25+ Foxp3+ T regulatory cells. |
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ISSN: | 0008-8749 1090-2163 |
DOI: | 10.1016/j.cellimm.2011.06.008 |