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学科主题临床医学
Sulfur dioxide inhibits excessively activated endoplasmic reticulum stress in rats with myocardial injury
Chen, Shanshan1; Du, Junbao1,2; Liang, Yinfang1; Ochs, Todd3; Liu, Die1; Zhu, Lulu1; Tang, Xiuying4; Tang, Chaoshu2,5; Jin, Hongfang1
关键词Sulfur Dioxide Isoproterenol Myocardial Injury Endoplasmic Reticulum Stress
刊名HEART AND VESSELS
2012-09-01
DOI10.1007/s00380-011-0192-7
27期:5页:505-516
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Cardiac & Cardiovascular Systems ; Peripheral Vascular Disease
研究领域[WOS]Cardiovascular System & Cardiology
关键词[WOS]UNFOLDED PROTEIN RESPONSE ; AIR-POLLUTION ; SERUM SULFITE ; ISOPROTERENOL ; HEART ; DYSFUNCTION ; METABOLISM ; INFARCTION ; APOPTOSIS ; NECROSIS
英文摘要

It has been demonstrated that excessively activated endoplasmic reticulum stress (ERS) is related to myocardial injury. The study was designed to explore the possible role of sulfur dioxide (SO2) in protecting excessively activated ERS in rats with isoproterenol (ISO)-induced myocardial injury. Wistar rats were randomly divided into control, ISO, and ISO + SO2 groups. Cardiac catheterization-derived hemodynamic parameters and myocardial enzymes in plasma were measured. Microstructure changes in myocardial tissues were examined. Cardiomyocyte apoptosis was detected by TUNEL method. Myocardial SO2 content and aspartate amino transferase (AAT) activity were detected. Meanwhile, protein and mRNA expressions of myocardial AAT1, AAT2, and ERS markers (GRP78, caspase-12, and CHOP) were evaluated. The results showed that cardiac function was decreased, myocardial microstructure was damaged, and myocardial enzyme levels and cardiomyocyte apoptosis were increased with a downregulated endogenous AAT/SO2 pathway, and that ERS markers were upregulated at transcriptional and translational levels in ISO-treated rats. However, the administration of an SO2 donor, resulting in an increased SO2 content in myocardial tissues, improved cardiac function and myocardial structure, and ameliorated myocardial enzyme levels and cardiomyocyte apoptosis associated with a downregulation of excessively activated ERS. In conclusion, the endogenous AAT/SO2 pathway was probably responsible for the inhibition of excessively activated ERS, which might be involved in the mechanism of ISO-induced myocardial injury.

语种英语
WOS记录号WOS:000308817200011
项目编号20070001702 ; 20070001770 ; 81070111 ; 30821001 ; 30801251 ; 2011CB503904 ; 7093136
资助机构Ministry of Education of China ; National Natural Science Foundation of China ; Major State Basic Research Development Program ; Natural Science Foundation of Beijing
引用统计
被引频次:10[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/55462
专题北京大学第一临床医学院_儿科
作者单位1.Northwestern Univ, Chicago, IL 60611 USA
2.Minist Educ, Key Lab Mol Cardiol, Beijing 100191, Peoples R China
3.Peking Univ, Hosp 1, Dept Pediat, Beijing 100034, Peoples R China
4.Peking Univ, Hosp 1, Dept Electron Microscope, Ctr Lab, Beijing 100034, Peoples R China
5.Peking Univ, Hlth Sci Ctr, Dept Physiol & Pathophysiol, Beijing 100191, Peoples R China
推荐引用方式
GB/T 7714
Chen, Shanshan,Du, Junbao,Liang, Yinfang,et al. Sulfur dioxide inhibits excessively activated endoplasmic reticulum stress in rats with myocardial injury[J]. HEART AND VESSELS,2012,27(5):505-516.
APA Chen, Shanshan.,Du, Junbao.,Liang, Yinfang.,Ochs, Todd.,Liu, Die.,...&Jin, Hongfang.(2012).Sulfur dioxide inhibits excessively activated endoplasmic reticulum stress in rats with myocardial injury.HEART AND VESSELS,27(5),505-516.
MLA Chen, Shanshan,et al."Sulfur dioxide inhibits excessively activated endoplasmic reticulum stress in rats with myocardial injury".HEART AND VESSELS 27.5(2012):505-516.
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