...
首页> 外文期刊>Archives of Toxicology >Arsenic-induced oxidative myocardial injury: protective role of arjunolic acid
【24h】

Arsenic-induced oxidative myocardial injury: protective role of arjunolic acid

机译:砷诱发的氧化性心肌损伤:芥酸的保护作用

获取原文
获取原文并翻译 | 示例
           

摘要

Arsenic, one of the most harmful metalloids, is ubiquitous in the environment. The present study has been carried out to investigate the protective role of a triterpenoid saponin, arjunolic acid (AA) against arsenic-induced cardiac oxidative damage. In the study, NaAsO2 was chosen as the source of arsenic. The free radical scavenging activity and the effect of AA on the intracellular antioxidant power were determined from its 2,2-diphenyl-1-picryl hydrazyl radical scavenging ability and ferric reducing/antioxidant power assay, respectively. Oral administration of NaAsO2 at a dose of 10 mg/kg body weight for 2 days caused significant accumulation of arsenic in cardiac tissues of the experimental mice in association with the reduction in cardiac antioxidant enzymes activities, namely superoxide dismutase, catalase, glutathione-S-transferase, glutathione reductase and glutathione peroxidase. Arsenic intoxication also decreased the cardiac glutathione (GSH) and total thiol contents and increased the levels of oxidized glutathione (GSSG), lipid peroxidation end products and protein carbonyl content. Treatment with AA at a dose of 20 mg/kg body weight for 4 days prior to NaAsO2 intoxication protected the cardiac tissue from arsenic-induced oxidative impairment. In addition to oxidative stress, arsenic administration increased total cholesterol level as well as the reduced high-density lipoprotein cholesterol level in the sera of the experimental mice. AA pretreatment, however, could prevent this hyperlipidemia. Histological studies on the ultrastructural changes in cardiac tissue supported the protective activity of AA also. Combining all, results suggest that AA could protect cardiac tissues against arsenic-induced oxidative stress probably due to its antioxidant property.
机译:砷是最有害的准金属之一,在环境中无处不在。本研究已经进行了研究,以研究三萜皂苷,阿魏酸(AA)对砷诱导的心脏氧化损伤的保护作用。在研究中,选择了NaAsO2 作为砷的来源。分别通过其2,2-二苯基-1-苦基肼基自由基清除能力和三价铁还原/抗氧化能力测定来确定自由基清除活性和AA对细胞内抗氧化能力的影响。口服NaAsO2 ”> (sub> ),但与实验性小鼠的心脏组织中砷的大量积累有关,这与心脏抗氧化酶(超氧化物歧化酶,过氧化氢酶,谷胱甘肽-S-转移酶,谷胱甘肽还原酶和谷胱甘肽过氧化物酶。砷中毒还降低了心脏的谷胱甘肽(GSH)和总硫醇含量,并增加了氧化型谷胱甘肽(GSSG),脂质过氧化终产物和蛋白质羰基含量的水平。在NaAsO2中毒前,以20 mg / kg体重的剂量AA处理4天,可保护心脏组织免受砷引起的氧化损伤。除氧化应激外,砷的施用增加了实验小鼠血清中的总胆固醇水平以及降低的高密度脂蛋白胆固醇水平。然而,AA预处理可以预防这种高脂血症。心脏组织超微结构变化的组织学研究也支持AA的保护活性。综合所有这些结果表明,AA可能由于其抗氧化特性而可以保护心脏组织免受砷诱导的氧化应激。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号