Institute of Life Sciences, University of Hyderabad Campus, Biology, Hyderabad 500 046, AP, India.
Phytomedicine. 2010 Jul;17(8-9):581-8. doi: 10.1016/j.phymed.2009.12.008. Epub 2010 Jan 22.
Although the anti-tumor effects of carvacrol have been demonstrated earlier, the exact underlying molecular mechanisms involved in its action have not been defined and in the present study an attempt has been made to identify the mechanism of carvacrol induced cell death in human metastatic breast cancer cells, MDA-MB 231.
Apoptosis induced by carvacrol was determined based on different assays like MTT assay, Annexin V, mitochondrial membrane potential assay, multicaspase activation assay and cell cycle analysis by flow cytometer. Cleavage of PARP, cytochrome c release and modulation of Bax and Bcl2 ratio by Western blot analysis were also studied.
The study clearly showed induction of apoptosis by carvacrol in MDA-MB 231 cells dose dependently at an IC(50) of 100 microM with a decrease in the mitochondrial membrane potential of the cells resulting in release of cytochrome c from mitochondria, caspase activation and cleavage of PARP.
The data in the present study clearly demonstrated anti-tumor effects of carvacrol on human metastatic breast cancer cells, MDA-MB 231, and that the compound could have a potential therapeutic significance in treating cancer.
虽然香芹酚的抗肿瘤作用已被证实，但它作用的确切潜在分子机制尚未确定，本研究试图确定香芹酚诱导人转移性乳腺癌细胞 MDA-MB 231 细胞死亡的机制。
根据 MTT 测定、Annexin V、线粒体膜电位测定、多半胱氨酸酶激活测定和流式细胞仪细胞周期分析等不同测定方法，确定香芹酚诱导的细胞凋亡。还通过 Western blot 分析研究了 PARP 的切割、细胞色素 c 释放以及 Bax 和 Bcl2 比值的调节。
研究结果清楚地表明，香芹酚在 MDA-MB 231 细胞中诱导细胞凋亡，呈剂量依赖性，IC（50）为 100μM，同时细胞线粒体膜电位下降，导致细胞色素 c 从线粒体中释放，半胱天冬酶激活和 PARP 切割。
本研究的数据清楚地表明香芹酚对人转移性乳腺癌细胞 MDA-MB 231 具有抗肿瘤作用，该化合物在治疗癌症方面可能具有潜在的治疗意义。
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