Int. J. Mol. Sci. 2013, 14(11), 22190-22201; doi:10.3390/ijms141122190
Article

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

Received: 12 August 2013; in revised form: 31 October 2013 / Accepted: 1 November 2013 / Published: 8 November 2013
(This article belongs to the Section Molecular Pathology)
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract: 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.
Keywords: myocardial ischemia/reperfusion injury; sulfur dioxide; preconditioning; mitogen activated protein kinase
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MDPI and ACS Style

Huang, P.; Sun, Y.; Yang, J.; Chen, S.; Liu, A.D.; Holmberg, L.; Huang, X.; Tang, C.; Du, J.; Jin, H. 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. Int. J. Mol. Sci. 2013, 14, 22190-22201.

AMA Style

Huang P, Sun Y, Yang J, Chen S, Liu AD, Holmberg L, Huang X, Tang C, Du J, Jin H. 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. International Journal of Molecular Sciences. 2013; 14(11):22190-22201.

Chicago/Turabian Style

Huang, Pan; Sun, Yan; Yang, Jinyan; Chen, Siyao; Liu, Angie D.; Holmberg, Lukas; Huang, Xiaomei; Tang, Chaoshu; Du, Junbao; Jin, Hongfang. 2013. "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." Int. J. Mol. Sci. 14, no. 11: 22190-22201.

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