Format

Send to

Choose Destination
J Cardiovasc Pharmacol. 2019 May;73(5):265-271. doi: 10.1097/FJC.0000000000000668.

Mechanism of Emulsified Isoflurane Postconditioning-Induced Activation of the Nrf2-Antioxidant Response Element Signaling Pathway During Myocardial Ischemia-Reperfusion: The Relationship With Reactive Oxygen Species.

Author information

1
Department of Anesthesiology, the Affiliated Hospital of Zunyi Medical College, Guizhou, China.
2
Key laboratory of anesthesia and organ protection, Zunyi Medical College, Guizhou, China.

Abstract

Emulsified isoflurane (EI) has been shown to alleviate myocardial ischemia-reperfusion (IR) injury. However, previous reports have not been focused on the underlying mechanism. We used models of IR injury in Langendorff-isolated rat hearts to determine the relationship between the mechanism underlying EI postconditioning (EIP)-induced activation of the nuclear factor-E2-related factor 2 (Nrf2)-antioxidant response element signaling pathway during myocardial IR, and its relationship with reactive oxygen species. In comparison with the IR group, the EIP group showed a significant reduction in myocardial ultrastructural damage, significant increase in function [heart rate, left ventricular developed pressure, left ventricular end-diastolic pressure, and maximal rate of the increase in left ventricular pressure (+dp/dtmax)], and upregulated expression of Nrf2, HO-I, NQO1, and SOD1 mRNA and proteins at the end of reperfusion. After treatment with N-(2-mercaptopropionyl)-glycine (MPG), the significant reduction in myocardial ultrastructural damage and significant increases in function, and mRNA and protein expression were no longer evident in the M + EIP group. These results show that EIP can regulate reactive oxygen species levels and activate the Nrf2-antioxidant response element signaling pathway, thereby attenuating myocardial IR injury in rats.

Supplemental Content

Full text links

Icon for Wolters Kluwer
Loading ...
Support Center