Department of Pediatrics, Peking University First Hospital, Beijing 100034, PR China.
Nitric Oxide. 2013 Aug 1;32:56-61. doi: 10.1016/j.niox.2013.04.008. Epub 2013 Apr 28.
The study was designed to explore if sulfur dioxide (SO2) preconditioning increased antioxidative capacity in rat with myocardial ischemia reperfusion (I/R) injury.
The myocardial I/R model was made by left coronary artery ligation for 30min and reperfusion for 120min in rats. Myocardial infarct size and plasma lactate dehydrogenase (LDH) and creatine kinase (CK) activities, plasma superoxide dismutase (SOD), malondialdehyde (MDA), glutathione peroxidase (GSH-Px) and glutathione (GSH) changes were detected for the rats. The contents of myocardial hydrogen sulfide (H2S) and nitric oxide (NO) were measured. Myocardial protein expressions of SOD1, SOD2, cystathionine γ-lyase (CSE) and iNOS were tested using Western blot.
Myocardial infarction developed and plasma CK and LDH activities were significantly increased in I/R group compared with those in control group, but SO2 preconditioning significantly reduced myocardial infarct size, and plasma CK and LDH activities. SO2 preconditioning successfully increased plasma SOD, GSH and GSH-Px levels and myocardial SOD1 protein expression, but decreased MDA level in rats of I/R group. Compared with controls, the myocardial H2S level and CSE expression were decreased after I/R, but myocardial NO level and iNOS expression were increased. With the treatment of SO2, myocardial H2S level and CSE expression were increased, but myocardial NO level and iNOS expression were decreased compared with those in I/R group.
SO2 preconditioning could significantly reduce I/R-induced myocardial injury in vivo in association with increased myocardial antioxidative capacity, upregulated myocardial H2S/CSE pathway but downregulated NO/iNOS pathway.
本研究旨在探讨二氧化硫（SO2）预处理是否增加了心肌缺血再灌注（I/R）损伤大鼠的抗氧化能力。
通过结扎大鼠左冠状动脉 30min 并再灌注 120min 建立心肌 I/R 模型。检测大鼠心肌梗死面积及血浆乳酸脱氢酶（LDH）和肌酸激酶（CK）活性、血浆超氧化物歧化酶（SOD）、丙二醛（MDA）、谷胱甘肽过氧化物酶（GSH-Px）和谷胱甘肽（GSH）的变化，测定心肌硫化氢（H2S）和一氧化氮（NO）含量。采用 Western blot 法检测心肌 SOD1、SOD2、胱硫醚γ-裂解酶（CSE）和诱导型一氧化氮合酶（iNOS）的蛋白表达。
与对照组相比，I/R 组大鼠发生心肌梗死，血浆 CK 和 LDH 活性明显升高，但 SO2 预处理显著减少了心肌梗死面积和血浆 CK 和 LDH 活性。SO2 预处理成功增加了 I/R 大鼠血浆 SOD、GSH 和 GSH-Px 水平及心肌 SOD1 蛋白表达，降低了 MDA 水平。与对照组相比，I/R 后大鼠心肌 H2S 水平和 CSE 表达降低，但心肌 NO 水平和 iNOS 表达升高。与 I/R 组相比，SO2 处理后大鼠心肌 H2S 水平和 CSE 表达增加，而心肌 NO 水平和 iNOS 表达降低。
SO2 预处理可显著减轻体内 I/R 诱导的心肌损伤，与增加心肌抗氧化能力、上调心肌 H2S/CSE 途径和下调 NO/iNOS 途径有关。
