中文摘要：

研究麦冬皂苷D（ophiopogonin D,OP-D）对阿霉素（doxorubicin,DOX）所致心肌损伤的保护作用。体外培养H9c2细胞,采用MTT法检测细胞毒性,MitoTracker探针法测定细胞内线粒体中活性氧（reactive oxygen species,ROS）含量,实时定量PCR和Western blotting分别检测ATF6α,GRP78和CHOP的mRNA及其蛋白表达。结果表明,DOX可诱导H9c2细胞内质网应激相关蛋白的表达量显著上升,并导致细胞活性氧ROS含量增加,细胞活力下降。而OP-D预处理可部分逆转DOX引起的上述变化,siRNA干扰促凋亡转录因子CHOP或抗氧化剂NAC预处理也有类似效应。此外,OP-D可明显减轻DOX所致小鼠心脏超微结构异常。这些结果说明,OP-D通过降低DOX诱导的ROS累积,进而缓解内质网应激而对心肌产生保护作用。

英文摘要：

This study aimed to examine whether ophiopogonin D （OP-D） is capable of protecting cardiomyocytes against DOX-induced injury and the mechanisms involved. H9c2 cells were cultured. MTT assay was used to evaluate cell viability and toxicity. Mito-tracker as fluorescence probe was used to measure ROS content raised from mitochondria. The mRNA and protein expression of ATF6a, GRP78 and CHOP were analyzed using real-time PCR and Western blotting, respectively. The results showed that a significant endoplasmic reticulum stress （ERS） was induced upon exposure of H9c2 cells to DOX as indicated by the increase in the expression of ERS related proteins, which was paralleled with the accumulation of reactive oxygen species （ROS） and decrease in the viability of H9c2 cells. Whereas, DOX-induced ROS accumulation and up-regulation of ERS related proteins were partially abolished by pretreatment with OP-D. Consequently,a DOX-induced ERS was mitigated by application of OP-D. Similarly, DOX-induced decrease in cell viability was partially attenuated by either inhibiting CHOP or pretreatment with N-acetylcysteine （NAC）, an antioxidant. Moreover, cardiac ultrastructural abnormalities seen in mouse receiving DOX injections were obviously ameliorated by pretreatment of OP-D. Taken together, the present study proved that OP-D protects cardiomyocytes against DOX-induced injury, at least in part, through reducing ROS accumulation and alleviating ERS.