title: Sulfur dioxide inhibits excessively activated endoplasmic reticulum stress in rats with myocardial injury.
abstract: 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 (SO(2)) in protecting excessively activated ERS in rats with isoproterenol (ISO)-induced myocardial injury. Wistar rats were randomly divided into control, ISO, and ISO + SO(2) 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 SO(2) 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/SO(2) pathway, and that ERS markers were upregulated at transcriptional and translational levels in ISO-treated rats. However, the administration of an SO(2) donor, resulting in an increased SO(2) 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/SO(2) pathway was probably responsible for the inhibition of excessively activated ERS, which might be involved in the mechanism of ISO-induced myocardial injury.
authors.affiliation: Department of Pediatrics, Peking University First Hospital, Xi-An Men Str No 1, West District, Beijing 100034, China.
authors.forename: Shanshan
authors.initials: S
authors.lastname: Chen
authors.forename: Junbao
authors.initials: J
authors.lastname: Du
authors.forename: Yinfang
authors.initials: Y
authors.lastname: Liang
authors.forename: Todd
authors.initials: T
authors.lastname: Ochs
authors.forename: Die
authors.initials: D
authors.lastname: Liu
authors.forename: Lulu
authors.initials: L
authors.lastname: Zhu
authors.forename: Xiuying
authors.initials: X
authors.lastname: Tang
authors.forename: Chaoshu
authors.initials: C
authors.lastname: Tang
authors.forename: Hongfang
authors.initials: H
authors.lastname: Jin
mesh_terms: D000818:Animals; D017209:Apoptosis; D004195:Disease Models, Animal; D059865:Endoplasmic Reticulum Stress / Q000187:drug effects*; D020287:In Situ Nick-End Labeling; D008297:Male; D015428:Myocardial Reperfusion Injury / Q000188:drug therapy / Q000378:metabolism* / Q000473:pathology; D032383:Myocytes, Cardiac / Q000378:metabolism* / Q000473:pathology; D051381:Rats; D017208:Rats, Wistar; D013458:Sulfur Dioxide / Q000494:pharmacology*
chemical_list: D013458:Sulfur Dioxide