L-(-)-表没食子儿茶素没食子酸酯对二甲基胂酸促小鼠肺肿瘤发生的抑制与其抑制氧化应激

Inhibition of (-) epigallocatechin gallate on dimethylarsinic acid promoting lung tumorigenesis through the induction of oxidative stress in mice

目的探讨抗氧化茶多酚L-(-)-表没食子儿茶素没食子酸酯[(-)epigallocatechin gallate,EGCG]对二甲基胂酸(dimethylarsinic acid,DMA(V))促小鼠肺肿瘤发生的抑制作用与氧化应激关系。方法利用4-硝基喹啉-1-氧化物(4-nitroquinoline 1-oxide,4NQO)作为始动剂,DMA(V)作为促进剂的致小鼠肺肿瘤两阶段动物模型。观察绿茶提取物中最有效的EGCG对DMA(V)致肿瘤发生的作用,同时通过高效液相色谱法(HPLC)测量小鼠肺中DNA氧化损伤的生物标志物8-氧-2’-脱氧鸟嘌呤核苷(8-oxo-2’-deoxyguanosine,8-oxodG)的变化。结果EGCG明显抑制4NQO与DMA(V)诱发小鼠肺肿瘤数(P<0.05)和肺组织中8-oxodG的生成(P<0.05)。结论EGCG对DMA(V)促肺肿瘤的抑制作用可能与其抑制氧化应激有关。

Objective To investigate inhibition of （（-） epigalloeatechin gallate, EGCG） on lung-tumor promotion and oxidative stress caused by administration of dimethylarsinic acid （DMA（V）） in mice. Methods The experimental animal model, which is induced by lung tumor initiator （4NQO） and promoter （DMA（V）） in mice, was used to examine the effect of EGCG on DMA（V） promoting lung tumorigenesis. The 8-oxo-2＇-deoxyguanosine（8-oxodG）analysis of lungs were used of HPLC. Results The incidence of lung tumors induced by lung tumor initiator （4NQO） and promoter（DMA（V） ） were, as well as 8-oxodG, suppressed by eotreatment with （-）epigallocateehin gallate（EGCG）. Conclusion EGCG can inhibit the tumor promotion, which is associated with its inhibition of oxidative stress induced by DMA.