Chen Chien-chang, Chen Yuhsin, Hsi Yi-Ting, Chang Chih-Sheng, Huang Li-Fen, Ho Chi-Tang, Way Tzong-Der, Kao Jung-Yie
Institute of Biochemistry, College of Life Science, National Chung Hsing University , Taichung, Taiwan 402.
J Agric Food Chem. 2013 Nov 27;61(47):11418-27. doi: 10.1021/jf4026184. Epub 2013 Nov 18.
In this study, we report that the essential oil obtained from Curcuma zedoaria Roscoe, known as zedoary, possesses efficient cytotoxic effects on non-small cell lung carcinoma (NSCLC) cells and causes cell apoptosis. Zedoary essential oil increased the sub-G1 population and the level of annexin-V binding and induced cleavage and activation of caspase-3, -8, and -9 and poly(ADP ribose) polymerase. Decreases in the levels of Bcl-2 and Bcl-xL and an increase in the Bax/Bcl-2 ratio were also observed following zedoary essential oil treatment. Notably, zedoary essential oil led to the release of AIF, endonuclease G, and cytochrome c into the cytosol and increased levels of p53 in H1299 cells. Our results indicate that zedoary essential oil slightly inhibited the phosphorylation of ERK1/2 and enhanced the phosphorylation of JNK1/2 and p38. Zedoary essential oil also inhibited AKT/NF-κB signaling pathways in H1299 cells. Moreover, intraperitoneal administration of zedoary essential oil significantly suppressed the growth of H1299 cells in vivo. In addition, potential active compounds were detected using gas chromatography and mass spectrometry. 8,9-Dehydro-9-formyl-cycloisolongifolene, 6-ethenyl-4,5,6,7-tetrahydro-3,6-dimethyl-5-isopropenyl-trans-benzofuran, eucalyptol, and γ-elemene were found in zedoary essential oil. In summary, our findings provide insight into the molecular mechanisms underlying zedoary essential oil-induced apoptosis in NSCLC cells that are worthy of further study.
在本研究中,我们报告称,从莪术(Curcuma zedoaria Roscoe)中提取的挥发油(即莪术油)对非小细胞肺癌(NSCLC)细胞具有有效的细胞毒性作用,并可导致细胞凋亡。莪术油增加了亚G1期细胞群体以及膜联蛋白V结合水平,并诱导了半胱天冬酶-3、-8和-9以及聚(ADP核糖)聚合酶的切割和激活。莪术油处理后还观察到Bcl-2和Bcl-xL水平降低以及Bax/Bcl-2比值升高。值得注意的是,莪术油导致凋亡诱导因子、核酸内切酶G和细胞色素c释放到细胞质中,并增加了H1299细胞中p53的水平。我们的结果表明,莪术油轻微抑制了ERK1/2的磷酸化,并增强了JNK1/2和p38的磷酸化。莪术油还抑制了H1299细胞中的AKT/NF-κB信号通路。此外,腹腔注射莪术油可显著抑制体内H1299细胞的生长。此外,使用气相色谱和质谱法检测到了潜在的活性化合物。在莪术油中发现了8,9-脱氢-9-甲酰基-环异长叶烯、6-乙烯基-4,5,6,7-四氢-3,6-二甲基-5-异丙烯基-反式苯并呋喃、桉叶油素和γ-榄香烯。总之,我们的研究结果为莪术油诱导NSCLC细胞凋亡的分子机制提供了见解,值得进一步研究。