The ERK1/2 signaling pathway is involved in sulfur dioxide preconditioning-induced protection against cardiac dysfunction in isolated perfused rat heart subjected to myocardial ischemia/reperfusion.
The ERK1/2 signaling pathway is involved in sulfur dioxide preconditioning-induced protection against cardiac dysfunction in isolated perfused rat heart subjected to myocardial ischemia/reperfusion.
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ERK1/2 信号通路参与二氧化硫预处理诱导的心肌缺血/再灌注大鼠离体灌注心脏功能障碍的保护作用。
DOI：
10.3390/ijms141122190
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发表时间：
2013-11-08
影响因子：
5.6
通讯作者：
Jin H
中科院分区：
文献类型：
--
作者：
Huang P;Sun Y;Yang J;Chen S;Liu AD;Holmberg L;Huang X;Tang C;Du J;Jin H
缺血/再灌注损伤（Ischemia/reperfusion injury，IRI）是心肌缺血再灌注过程中的常见损伤，预处理被认为是预防心肌缺血再灌注损伤的最佳策略之一。我们以前的研究表明，小剂量的二氧化硫（SO2）作为预处理可发挥心脏保护作用。然而，潜在的心脏保护机制仍不清楚。本研究旨在探讨细胞外调节蛋白激酶1/2（ERK 1/2）信号通路是否介导SO2预处理对离体大鼠缺血/再灌注（I/R）心功能不全的保护作用。在体外进行Langendorff心脏灌注，其中56只雄性Wistar大鼠随机分为7组：对照组、5 μmol/L SO2组（S5）、2-（2-氨基-3-甲氧基苯基）-4H-1-苯并吡喃-4-酮（PD 98059）+ 5 μmol/L SO2（PD 98059 + S5）组、PD 98059组、I/R组、5 μmol/L SO2 + I/R（S5 + I/R）组和PD 98059 + 5 μmol/L SO2 + I/R（PD 98059 + S5 + I/R）组。检测心功能和心肌磷酸化ERK 1/2蛋白。我们发现，在离体大鼠心脏I/R导致心功能不全与磷酸化ERK 1/2蛋白的显着增加。SO2预处理可显著抑制心肌缺血再灌注后ERK 1/2蛋白磷酸化，改善心功能（p < 0.05）。而PD 98059预处理可防止SO2预处理的上述效应。结论：SO2预处理可通过抑制ERK 1/2信号通路的过度激活，减轻大鼠离体心脏I/R后的心功能障碍。
Ischemia/reperfusion injury (IRI) occurs frequently during reperfusion of ischemic myocardium, and preconditioning has been regarded as one of the best strategies to prevent myocardial injury during the ischemia/reperfusion process. Our previous studies indicated that a small dose of sulfur dioxide (SO2) used as preconditioning exerts cardioprotection. However, the mechanisms underlying the cardioprotection remain unclear. The present study was designed to examine if the extracellular regulated protein kinases 1/2 (ERK1/2) signaling pathway mediated protection against cardiac dysfunction after SO2 preconditioning in isolated rat hearts subjected to ischemia/reperfusion (I/R). Langendorff heart perfusion was performed in vitro, where 56 male Wistar rats were randomly divided into seven groups: control group, 5 μmol/L SO2 group (S5), 2-(2-Amino-3-methoxyphenyl)-4H-1-benzopyran-4-one (PD98059) + 5 μmol/L SO2 (PD98059 + S5) group, PD98059 group, I/R group, 5 μmol/L SO2 + I/R (S5 + I/R) group and PD98059 + 5 μmol/L SO2 + I/R (PD98059 + S5 + I/R) group. Cardiac function and myocardial phosphorylated ERK1/2 protein were measured. We found that I/R in isolated rat heart resulted in cardiac dysfunction with a significant increase in phosphorylated ERK1/2 protein. SO2 preconditioning markedly suppressed phosphorylated ERK1/2 protein and improved cardiac function in isolated rat heart with I/R (p < 0.05). However, pre-treatment with PD98059 could prevent the above effects of SO2 preconditioning. In conclusion, SO2 preconditioning protected against cardiac dysfunction in isolated rat heart subjected to I/R via suppression of the over-activation of the ERK1/2 signaling pathway.
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影响因子：
4.1
作者：
Punn, A;Mockridge, JW;Heads, RJ
通讯作者：
Heads, RJ
影响因子：
6.7
作者：
Chung, Ji Won;Choi, Ran Joo;Kim, Yeong Shik
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Kim, Yeong Shik
影响因子：
5
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Du, Junbao
DOI：
10.1073/pnas.92.17.7686
发表时间：
1995-08-15
影响因子：
11.1
作者：
DUDLEY, DT;PANG, L;SALTIEL, AR
通讯作者：
SALTIEL, AR
影响因子：
4.5
作者：
Bai, JL;Meng, ZQ
通讯作者：
Meng, ZQ