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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.

J Cardiovasc Pharmacol. 2019 May;73(5):265-271

Authors: Chen W, Chen XY, Wang Y, Wang HY, Zhou WJ, Yu T

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.

PMID: 31082959 [PubMed – in process]

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