Sevoflurane preconditioning alleviates hypoxia-reoxygenation-induced myocardial injury via regulating the MIR210HG/miR-377-3p/PUM2 axis
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Published on: April 19, 2011
Lu Gan1, Xiaobing Du1, Lu Lu1
1Department of Anesthesiology, The Affiliated Hospital of Hebei University, Baoding City, Hebei Province, 071000, China.
Background:
Sevoflurane preconditioning (SPC) is a common protective strategy against myocardial ischemia-reperfusion injury (MI/RI). MIR210HG is a hypoxia-induced long non-coding RNA and involves multiple molecular pathways.
Objectives:
The study investigated the role of MIR210HG in the improvement of MI/RI by SPC.
Materials And Methods:
In vitro, AC16 cells underwent hypoxia-reoxygenation (H/R). Cell viability was tested via CCK-8. Inflammatory cytokines, myocardial injury markers and key enzymes in glycolysis were measured by ELISA. Superoxide dismutase (SOD) and malondialdehyde (MDA) concentrations were detected to assess cellular oxidative stress. RNA immunoprecipitation (RIP) and luciferase reporter assays verified the target relationship.
Results:
In AC16 cells, MIR210HG level rises with prolonged H/R treatment but is inhibited by SPC. Elevated MIR210HG counteracted sevoflurane's protection against H/R-induced myocardial injury through enhancing viability, inhibiting inflammation and oxidative stress. SPC regulated glycolytic metabolism and key enzyme activity independent of MIR210HG. miR-377-3p reversed MIR210HG's role, and PUM2 was its direct target.
Conclusion:
MIR210HG/miR-377-3p/PUM2 axis as a key downstream mediator of sevoflurane preconditioning against MI/RI through mediating oxidative stress and inflammatory response.
