Abstract
The current drugs against sleeping sickness are derived from cancer chemotherapeutic approaches. Herein, we aimed at evaluating the in vitro effect of alcoholic extracts of Artemisia annua (AMR), Rumex abyssinicus (RMA), and Catha edulis Forsk (CEF) on proliferation/viability of 1321N1 astrocytoma, MCF-7 breast cancer, THP-1 leukemia, and LNCaP, Du-145, and PC-3 prostate cancer cells and on Trypanosoma brucei cells. Proliferation of tumor cells was evaluated by WST-1 assay and viability/behaviour of T. brucei by cell counting and light microscopy. CEF was the most efficient growth inhibitor in comparison to AMR and RMA. Nevertheless, in LNCaP and THP-1 cells, all extracts significantly inhibited tumor growth at 3 μg/mL. All extracts inhibited proliferation of T. brucei cells in a concentration-dependent manner. Microscopic analysis revealed that 95% of the T. brucei cells died when exposed to 33 μg/mL CEF for 3 hrs. Similar results were obtained using 33 μg/mL AMR for 6 hrs. In case of RMA, however, higher concentrations were necessary to obtain similar effects on T. brucei. This demonstrates the antitumor efficacy of these extracts as well as their ability to dampen viability and proliferation of T. brucei, suggesting a common mechanism of action on highly proliferative cells, most probably by targeting cell metabolism.
Highlights
Many anticancer reagents, including nucleotide analogues and other DNA synthesis inhibitors, aim at exerting a specific activity against rapidly proliferating cell types
In addition to LNCaP prostate cancer cells, Catha edulis Forsk (CEF) best inhibits THP-1 leukemia and MCF7 cells when applied at concentrations ≥33 μg/mL
Results demonstrated that CEF inhibited proliferation of T. brucei cells at the last two higher dilutions (166 and 333 μg/mL), and its initial effect was observed within the first hour of incubation, and its maximum effect was seen at the 6th hr (Figure 4(a) and Table 1)
Summary
Many anticancer reagents, including nucleotide analogues and other DNA synthesis inhibitors (e.g., methotrexate), aim at exerting a specific activity against rapidly proliferating cell types. It is estimated that at least 300 000 ± 500 000 people are presently infected [5] This burden of the disease, all the available drugs have a number of shortcomings during treatment because of resistance development against them, allergic reactions, undesirable effects in the urinary tract, and reactive encephalopathy (with 3–10% fatality), ISRN Biochemistry and some regimens are strict and difficult to apply [6]. This raises an urgent need for novel, safe, rapidly-acting, and inexpensive agents for the treatment of HAT [7]
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