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.
*Department of Anesthesiology, the Affiliated Hospital of Zunyi Medical College, Guizhou, China; and
†Key laboratory of anesthesia and organ protection, Zunyi Medical College, Guizhou, China.
Reprints: Hai-Ying Wang, MD, Department of Anesthesiology, the Affiliated Hospital of Zunyi Medical College, Dalian Rd, Huichuan District, Zunyi 563000, Guizhou Province, China (e-mail: email@example.com).
The National Natural Sciences Foundation of China (reference: 30960366).
The authors report no conflicts of interest.
W. Chen and X.-Y. Chen contributed equally to this article.
Received December 06, 2018
Accepted February 04, 2019