绿原酸诱导肺癌细胞凋亡及其机制研究  

Effect of Chlorogenic Acid on Lung Cancer A549 Cell Apoptosis and Mechanism

作　　者：田伟[1] 豆亚伟[1] 王宏涛[1] 朱建飞[1] 戴云罗 向晖[1] 

机构地区：[1]陕西省人民医院胸外科,西安710068

出　　处：《解放军预防医学杂志》2016年第6期854-857,共4页Journal of Preventive Medicine of Chinese People's Liberation Army

摘　　要：目的研究绿原酸对人肺癌A549细胞凋亡的作用及其机制,为临床应用提供依据。方法四氮唑盐(MTT)法检测不同浓度的绿原酸对A549细胞增殖的影响;流式细胞术检测细胞凋亡率;采用间接荧光标记法测定细胞内活性氧水平的变化;分光光度法检测绿原酸对表皮生长因子受体酪氨酸激酶(epidermal growth factor receptor tyrosine kinase,EGFR-TPK)、基质金属蛋白酶(matrix metalloproteinase 2,MMP-2)和氨肽酶N(aminopeptidase,APN)活性的变化。结果MTT法检测显示,绿原酸在24 h、48 h和72 h时均可抑制A549细胞增殖,且呈浓度和时间依赖性关系趋势;绿原酸作用48 h后,细胞凋亡率呈现明显增高的趋势,与对照组比较差异有显著性(P<0.01);在100μg/ml质量浓度的绿原酸作用下使细胞内活性氧(ROS)百分率达到了(42.32±3.3)%,与对照组相比比较差异有显著性(P<0.01);绿原酸对APN、EGFR-TPK和MMP-2半数抑制浓度(IC_(50))分别为(8.12±0.78)、(29.43±2.76)和(1.54±0.13)μg/ml,显示出了较好的抑制效果。结论绿原酸可以抑制A549的增殖和转移,促进细胞凋亡,其凋亡机制可能与细胞内活性氧组分的增多及APN、EGFR-TPK和MMP-2活性降低有关。Objective To study the effect of chlorogenic acid on apoptosis of lung cancer A549 cells and its mechanism. Methods MTT assay was used to detect the cell proliferation induced by chlorogenic acid. Using the indirect fluorescent marker method, the reactive oxygen species （ROS） in cells was monitored by flow cytometry. The inhibitory effect of？ chlorogenic acid on EGFR-TPK, APN, and MMP-2 was detected using spectrophotometric method. Results Chlorogenic acid inhibited the cell proliferation in a time- and concentration-dependent manner. After treatment with chlorogenic acid, the cell apoptosis rate and ROS activation rate were significantly increased （ P〈0.01 ）. The half inhibition rate IC50 of chlorogenic acid on APN, EGFR- TPK and MMP-2 was （8.12± 0.78） ,（29.43 ± 2.76） and （1.54±0.13） μg/ml respectively. Conclusion Chlorogenic acid can inhibit A549 cell proliferation and induce apoptosis, which may be associated with the generation of ROS and decreased ac- tivity of APN, EGFR-TPK and MMP-2.

关 键 词：绿原酸 人肺癌A549 凋亡 活性氧组分 表皮生长因子受体酪氨酸激酶 基质金属蛋白酶 氨肽酶N 

分 类 号：R734.2[医药卫生—肿瘤]