摘要
本研究采用小鼠腹腔注射法CdCl_2[1 mg/(kg·d)]和不同剂量的CAPE,处理7 d构建镉染毒小鼠模型,利用光镜技术直观的反映镉致心脏组织形态学的改变,并测定NO含量及金属螯合实验探讨CAPE对镉致损伤的保护机制。结果显示,镉的毒性作用能够引起损伤组心脏空泡增多,炎症细胞侵润及心肌细胞肿胀,而CAPE能够减少空泡的形成及心肌细胞肿胀等;另外,CAPE能够剂量依赖的螯合Fe^2+,主要与其结构中邻苯二酚结构有关。结果表明,镉能够通过抑制NO的释放,改变心肌细胞的正常形态,损伤其正常的机能,而CAPE的保护作用可能是通过螯合金属离子,起到类似金属硫蛋白的作用。
This assay was designed to study the effect of caffeic acid phenethyl ester （CAPE） on cadmium （Cd）-in- dueed mice cardiac damage. Mice were treated by i. p. given CdC12 [ 1 mg/（kg , d） ] and different doses of CAPE for 7 days,the cardiac histopathological change induced by cadmium was observed using light microscope and the action mechanism of CAPE against the toxicity of Cd was exploited by NO content determination and metal chelating assay. The data showed that the intoxication of Cd can lead to the increase of vacuolns, the infiltration of inflammatory cells and the swelling of myocytes in the damage group, however, the protective effect of CAPE can reduce the occurrence of the his- topathologieal changes. Moreover, CAPE can chelate with Fe2 ~ in a dose-dependent manner, probably relating to its eate- chol molecule. It was indicated that Cd can change its normal structure of myocytes and result in the cardiac damage. In addition,beside antioxidative effect,the mechanism for the protective effect of CAPE may owe to its metal chelating abili- ty to reduce the damage to biological macromolecules, acting as the role of metallothionein.
出处
《天然产物研究与开发》
CAS
CSCD
北大核心
2013年第9期1274-1276,共3页
Natural Product Research and Development
基金
林业公益性行业科研专项(200904004)
陕西省自然科学基金项目(2012JQ2011)
陕西省教育厅自然科学基金项目(12JK0712,12JK0623)
西安市未央区项目(201112,201209)
关键词
镉
咖啡酸苯乙酯
一氧化氮
金属螯合
心脏形态学改变
cadmium
caffeic acid phenethyl ester
NO
chelating ability
cardiac histopathologieal change
