摘要
目的研究儿茶素〔(+)catechin〕对氧化应激引起的鼠小胶质细胞N9DNA损伤的保护作用。方法以叔丁基过氧化氢(tBHP)损伤N9细胞为氧化应激模型,采用MTT法、流式细胞分析法、Cometassay(彗星实验分析)及WesternBlot法。结果儿茶素明显地抑制tBHP诱导鼠小胶质细胞死亡,且在低浓度范围内呈剂量依赖性;流式分析结果表明,(+)catechin有效地清除细胞内过量的自由基;经彗星实验验证,tBHP诱导的DNA损伤被(+)catechin显著地抑制。蛋白印迹结果显示poly(ADPribose)polymerase(PARP)的表达量随着(+)catechin给药浓度的增加而增加,而p53的表达无明显改变。结论(+)catechin对氧化应激损伤的N9细胞具有保护作用,其机制可能与降低细胞内自由基(ROS)的含量,增加PARP的表达进而修复受损的DNA有关。
Aim To study the protective effect of （ ＋ ）-catechin on N9 cell DNA damage induced by oxidative stress. Methods The oxidative cellular responses were method, flow were applied. induced by cytomytric Results exposure to tBHP. MTI＇ analysis, and Western Blot （ ＋ ）-catechin significantly inhibited tBHP-induced N9 cell death in a dose-dependent manner at the lower doses ranging from 0. 063 to 0. 25 mmol · L^-1. The results of flow cytomytric analysis indicated that （ ＋ ）-catechin effectively scavenged excess intracellular ROS. Comet assay confirmed that （ ＋ ）-catechin markedly blocked tBHP-induced DNA damage. Furthermore, with increased doses of （ ＋ ）-catechin, the expression of PARP was significantly enhanced, but p53 remained stable and p-p53 proteins expression decreased. Conchtsion （ ＋ ）- catechin has the protective effect against N9 cell impairment induced by oxidative stress. The defensive mechanism may be related with the effect of ROS scavenging and increased expression of PARP, which repaires DNA damage.
出处
《中国药理学通报》
CAS
CSCD
北大核心
2005年第12期1520-1523,共4页
Chinese Pharmacological Bulletin
