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

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


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