Abstract
The present study aims at defining the differential cytotoxicity effect of artemisinin toward P815 (murin mastocytoma) and BSR (kidney adenocarcinoma of hamster) cell lines. Cytotoxicity was measured by the growth inhibition using MTT assay. These in vitro cytotoxicity studies were complemented by the determination of apoptotic DNA fragmentation and Annexin V- streptavidin-FITC assay. Furthermore, we examined the in vitro synergism between artemisinin and the chemotherapeutic drug, vincristin. The in vivo study was investigated using the DBA2/P815 (H2d) mouse model. While artemisinin acted on both tumor cell lines, P815 was much more sensitive to this drug than BSR cells, as revealed by the respective IC50 values (12 µM for P815 and 52 µM for BSR cells). On another hand, and interestingly, apoptosis was induced in P815 but not induced in BSR. These data, reveal an interesting differential cytotoxic effect, suggesting the existence of different molecular interactions between artemisinin and the studied cell lines. In vivo, our results clearly showed that the oral administration of artemisinin inhibited solid tumor development. Our study demonstrates that artemisinin caused differential cytotoxic effects depending not only on the concentration and time of exposure but also on the target cells.
Highlights
Artemisia annua L., a Chinese medicinal herb has evoked wide interest for its artemisinin content
The present study aims at defining the differential cytotoxicity effect of artemisinin toward P815 and BSR cell lines
The concentrations leading to 50 % cytotoxicity (IC50) were about 12 and 52 lM for P815 and BSR cell lines, respectively
Summary
Artemisia annua L., a Chinese medicinal herb has evoked wide interest for its artemisinin content. This sesquiterpene lactone compound contains an endoperoxide bridge that forms a carbon-base free radical, when encountering an iron atom [1, 2]. The artemisinin molecule contains an endoperoxide bridge (–C–O–O–C–) that interacts with Fe(II) to form free radicals [1, 2]. Because malaria parasites contain a high amount of Fe(II) in the form of heme molecules [5], artemisinin’s anti-malarial bioactivity is due to its reaction with the intra-parasitic iron source and the generation of free radicals leading to cellular destruction [2, 6]
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