Jayathilake Abilasha Gayani, Senior Paul Vincent, Su Xiao Qun
Centre for Chronic Disease, College of Health and Biomedicine, Victoria University, P.O. Box 14428, Melbourne, VIC, 8001, Australia.
Melbourne Medical School Western Campus, Western Centre for Health Research and Education, Sunshine Hospital, St Albans, VIC, 3021, Australia.
BMC Complement Altern Med. 2016 Aug 30;16(1):328. doi: 10.1186/s12906-016-1311-x.
Colorectal cancer (CRC) is the third most common cancer in the world. The current available treatments for CRC include surgery, chemotherapy and radiotherapy. However, surgery is only useful when the disease is diagnosed at the earlier stage. Chemotherapy and radiotherapy are associated with numerous side effects that decrease the patients' quality of life. Safer, effective alternatives, such as natural compounds, to chemotherapy are desirable. This study assessed the efficacy of free fatty acid (FFA) extract of krill oil on three human CRC cells lines.
HCT-15, SW-480 and Caco-2 cells were treated with the FFA extracts of krill oil and fish oil for 48 h while treatments with the bioactive omega-3 polyunsaturated fatty acids (LC n-3 PUFA) of these marine oils, eicosapentaenoic acid (EPA, C20:5n-3) and docosahexaenoic acid (DHA, C22:6n-3) in comparison with a n-6 PUFA, arachnoid acid (AA, C20:4n-6) were up to 72 h at the concentrations of 50, 100, 150 and 200 μM. Effects of all the treatments on cell proliferation were assessed using a water-soluble tetrazolium-1 (WST-1) assay kit at 24, 48 and 72 h. Effects of FFA extract of krill oil and EPA on apoptosis and mitochondrial membrane potential were determined using commercial kits after 48 h of treatment.
Krill oil extract inhibited cell proliferation of all three cell lines in the similar manner as fish oil extract. A significant cell apoptosis and increase in mitochondrial membrane potential were observed after the treatment with krill oil extract. EPA at the concentration of 200 μM reduced significantly the proliferation of HCT-15 and SW-480 at 24, 48 and 72 h. In addition, EPA treatment (100 and 200 μM) resulted in significant cell apoptosis in all three cell lines. No significant changes were observed after treatment with DHA and AA.
Our results indicate that the FFA extract of krill oil maybe an effective chemotherapeutic agent to suppress proliferation and induce apoptosis in CRC cells through its bioactive constitute EPA. Although the exact mechanism of the pro-apoptotic properties of krill oil extract is unclear, mitochondrial pathway seems to be implicated.
结直肠癌（CRC）是全球第三大常见癌症。目前CRC的可用治疗方法包括手术、化疗和放疗。然而，手术仅在疾病早期诊断时有用。化疗和放疗会带来许多副作用，降低患者的生活质量。因此，需要更安全、有效的替代方法，如天然化合物，来替代化疗。本研究评估了磷虾油游离脂肪酸（FFA）提取物对三种人CRC细胞系的疗效。
用磷虾油和鱼油的FFA提取物处理HCT-15、SW-480和Caco-2细胞48小时，同时用这些海洋油中的生物活性ω-3多不饱和脂肪酸（LC n-3 PUFA），即二十碳五烯酸（EPA，C20:5n-3）和二十二碳六烯酸（DHA，C22:6n-3）与一种n-6多不饱和脂肪酸花生四烯酸（AA，C20:4n-6）在50、100、150和200μM浓度下处理长达72小时。在24、48和72小时使用水溶性四氮唑-1（WST-1）检测试剂盒评估所有处理对细胞增殖的影响。处理48小时后，使用商业试剂盒测定磷虾油FFA提取物和EPA对细胞凋亡和线粒体膜电位的影响。
磷虾油提取物以与鱼油提取物相似的方式抑制所有三种细胞系的细胞增殖。用磷虾油提取物处理后观察到显著的细胞凋亡和线粒体膜电位增加。浓度为200μM的EPA在24、48和72小时显著降低了HCT-15和SW-480的增殖。此外，EPA处理（100和200μM）导致所有三种细胞系发生显著的细胞凋亡。用DHA和AA处理后未观察到显著变化。
我们的结果表明，磷虾油的FFA提取物可能是一种有效的化疗药物，通过其生物活性成分EPA抑制CRC细胞增殖并诱导凋亡。尽管磷虾油提取物促凋亡特性的确切机制尚不清楚，但线粒体途径似乎与之有关。
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