太白楤木皂苷对砷诱导的肝细胞线粒体途径凋亡的保护作用  

Protection of saponin from Aralia taibaiensis on the mitochondria dependent apoptosis induced by arsenic exposure

作　　者：李影娜[1] 章琳[1] 奚苗苗[2] 崔大江[1] 杨渭临[1] 秦绪军[3] 

机构地区：[1]西安交通大学第二附属医院老年病科,西安710004 [2]第四军医大学西京医院药剂科,西安710032 [3]第四军医大学预防医学院毒理学教研室,陕西省自由基生物学与医学重点实验室,第四军医大学抗氧化损伤防治研究中心,西安710032

出　　处：《中南药学》2013年第8期576-580,共5页Central South Pharmacy

基　　金：陕西省中医药管理局课题(No.zy35);国家自然科学基金(No.31070766);陕西省科技新星项目(No.2010KJXX-06)

摘　　要：目的探讨太白楤木皂苷对砷暴露损伤的保护作用及分子机制。方法人正常肝细胞HL-7702进行砷暴露及太白楤木皂苷保护处理。砷暴露组用10μmol L-1终浓度的NaAsO2处理,太白楤木皂苷保护组用不同浓度太白楤木皂苷预处理12 h后,再进行砷暴露处理。24 h后MTT法检测细胞活力;12 h后收集细胞样品,分别检测细胞的凋亡、活性氧(ROS)、还原型谷胱甘肽(GSH),氧化损伤产物丙二醛(MDA)水平以及线粒体凋亡途径的重要因子细胞色素C(Cyto C)释放和Caspase-3的激活情况。结果砷暴露可以引起肝细胞活力显著降低,给予不同浓度的太白楤木皂苷具有一定的保护作用,其中5μg mL-1太白楤木皂苷保护效果最佳。砷暴露可以引起细胞凋亡比例显著增加,细胞ROS水平升高,GSH水平降低,氧化损伤产物MDA水平增加,线粒体凋亡途径因子Cyto C和Caspase-3的激活。太白楤木皂苷(5μg mL-1)预处理能够显著拮抗砷暴露引起的细胞上述指标变化。结论砷暴露可以通过诱导细胞氧化应激,激活线粒体途径细胞凋亡,发挥其损伤毒性作用。太白楤木皂苷可以通过抑制细胞氧化应激,抑制线粒体途径的细胞凋亡,从而发挥其抗砷暴露损伤的保护作用。Objective To evaluate the protection of saponin from Aralia taibaiensis on the cellular damage induced by arsenic exposure.Methods Human normal liver cell line HL-7702 was exposed to 10 μmol L-1sodium arsenite.For the protection groups,the cells were pre-incubated with different concentrations of saponin for 12 h before subsequent treatment of arsenic.The cell viability was determined by MTT assay 24 h after the arsenic exposure and 12 h after the arsenic exposure,the cells were collected to detect the levels of cell apoptosis,reactive oxygen species（ROS）,reduced glutathione（GSH）,malondialdehyde（MDA）,release of Cytochrome C（Cyto C）,and activation of Caspase-3.Results Arsenic exposure significantly decreased the cell viability,in which saponin showed efficient protection,especially at the concentration of 5 μg mL-1.Further results showed that arsenic exposure significantly induced the increased cell apoptosis,the increased ROS and MDA levels,as well as the decreased GSH level in the cells.At the same time,arsenic exposure also stimulated the release of Cyto C and the activation of Caspase-3.Pre-treatment of saponin（5 μg mL-1） almost abolished the above changes induced by arsenic exposure.Conclusion Arsenic exposure induced oxidative stress may activat the mitochondria dependent apoptosis.Saponin treatment shows effective protection by inhibiting the oxidative stress,the release of Cyto C and the activation of Caspase-3,and finally the mitochondria dependent apoptosis induced by arsenic exposure.

关 键 词：太白楤木 皂苷 砷 线粒体 凋亡 保护作用 

分 类 号：R966[医药卫生—药理学] R285.5[医药卫生—药学]