Leong Lek Mun, Chan Kok Meng, Hamid Asmah, Latip Jalifah, Rajab Nor Fadilah
Biomedical Science Programme, School of Diagnostic and Applied Health Science, Faculty of Health Sciences, Universiti Kebangsaan Malaysia, Jalan Raja Muda Abdul Aziz, 50300 Kuala Lumpur, Malaysia.
Environmental Health and Industrial Safety Programme, School of Diagnostic and Applied Health Science, Faculty of Health Sciences, Universiti Kebangsaan Malaysia, Jalan Raja Muda Abdul Aziz, 50300 Kuala Lumpur, Malaysia; Toxicology Laboratory, Faculty of Health Sciences, Universiti Kebangsaan Malaysia, Jalan Raja Muda Abdul Aziz, 50300 Kuala Lumpur, Malaysia.
Evid Based Complement Alternat Med. 2016;2016:2091085. doi: 10.1155/2016/2091085. Epub 2016 Jan 17.
The use of herbal formulations has gained scientific interest, particularly in cancer treatment. In this study, the herbal formulation of interest, denoted as C168, is a mixture of eight genera of plants. This study aims to investigate the antiproliferative effect of C168 methanol extract (CME) on various cancer cells and its underlying mechanism of action on the most responsive cell line, namely, HCT 116 cells. CME exerted antiproliferative activities on HCT 116 colorectal carcinoma cells and HepG2 hepatocellular carcinoma cells but not on CCD-841-CoN normal colon epithelial cells, Jurkat E6.1 lymphoblastic leukemic cells, and V79-4 Chinese hamster lung fibroblasts. Further investigation on HCT 116 cells showed that CME induced G2/M cell-cycle arrest and apoptosis. Treatment of CME induced oxidative stress in HCT 116 cells by increasing the superoxide anion level and decreasing the intracellular glutathione. CME also increased tail moment value and H2AX phosphorylation in HCT 116 cells, suggesting DNA damage as an early signal of CME induced apoptosis. Loss of mitochondrial membrane potential in CME-treated cells also indicated the involvement of mitochondria in CME induced apoptosis. This study indicated the selectivity of CME toward colon cancer cells with the involvement of oxidative damage as its possible mechanism of action.
草药配方的应用已引起科学关注,尤其是在癌症治疗方面。在本研究中,所关注的草药配方C168是八种植物属的混合物。本研究旨在探究C168甲醇提取物(CME)对各种癌细胞的抗增殖作用及其对最敏感细胞系即HCT 116细胞的潜在作用机制。CME对HCT 116结肠癌细胞和HepG2肝癌细胞具有抗增殖活性,但对CCD - 841 - CoN正常结肠上皮细胞、Jurkat E6.1淋巴细胞白血病细胞和V79 - 4中国仓鼠肺成纤维细胞没有作用。对HCT 116细胞的进一步研究表明,CME诱导G2/M期细胞周期阻滞和细胞凋亡。CME处理通过提高超氧阴离子水平和降低细胞内谷胱甘肽水平诱导HCT 116细胞产生氧化应激。CME还增加了HCT 116细胞的尾矩值和H2AX磷酸化,表明DNA损伤是CME诱导细胞凋亡的早期信号。CME处理的细胞中线粒体膜电位的丧失也表明线粒体参与了CME诱导的细胞凋亡。本研究表明CME对结肠癌细胞具有选择性,氧化损伤可能是其作用机制。