黄花蒿、阿比西尼亚和长春花提取物对肿瘤和布鲁氏锥虫细胞体外抑制作用的研究。

ISRN biochemistry Pub Date : 2013-09-22 eCollection Date: 2013-01-01 DOI:10.1155/2013/910308
Netsanet Worku, Andualem Mossie, August Stich, Arwid Daugschies, Susanne Trettner, Nasr Y A Hemdan, Gerd Birkenmeier
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引用次数: 27

摘要

目前治疗昏睡病的药物来源于癌症化疗方法。本实验旨在研究青蒿(Artemisia annua, AMR)、阿比sinicus (RMA)和Catha edulis Forsk (CEF)酒精提取物对1321N1星形细胞瘤、MCF-7乳腺癌、THP-1白血病、LNCaP、Du-145和PC-3前列腺癌细胞和布鲁氏锥虫细胞增殖/活力的体外影响。采用WST-1法观察肿瘤细胞的增殖情况,采用细胞计数和光镜观察布鲁氏t细胞的活力/行为。与AMR和RMA相比,CEF是最有效的生长抑制剂。然而,在LNCaP和THP-1细胞中,所有提取物在3 μg/mL时均显著抑制肿瘤生长。所有提取物均具有浓度依赖性地抑制布鲁氏体细胞的增殖。显微镜分析显示,在33 μg/mL CEF作用3小时后,95%的布鲁氏t细胞死亡。用33 μg/mL AMR作用6小时,结果相似。然而,在RMA的情况下,需要更高的浓度才能对布氏体产生类似的效果。这证明了这些提取物的抗肿瘤功效以及它们抑制T. brucei的活力和增殖的能力,表明它们对高增殖细胞的共同作用机制,最有可能是通过靶向细胞代谢。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Evaluation of the In Vitro Efficacy of Artemisia annua, Rumex abyssinicus, and Catha edulis Forsk Extracts in Cancer and Trypanosoma brucei Cells.

Evaluation of the In Vitro Efficacy of Artemisia annua, Rumex abyssinicus, and Catha edulis Forsk Extracts in Cancer and Trypanosoma brucei Cells.

Evaluation of the In Vitro Efficacy of Artemisia annua, Rumex abyssinicus, and Catha edulis Forsk Extracts in Cancer and Trypanosoma brucei Cells.

Evaluation of the In Vitro Efficacy of Artemisia annua, Rumex abyssinicus, and Catha edulis Forsk Extracts in Cancer and Trypanosoma brucei Cells.

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.

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