Precondition of Sevoflurane Upregulates TIMP3 Expression to Alleviate Myocardial Ischemia/Reperfusion Injury
Background
Previous studies have pointed out that sevoflurane (Sef) preconditioning could relieve myocardial ischemia/reperfusion (I/R) injury, but the mechanisms is still unknown.
Methods
C57BL/6 mice model of myocardial I/R injury was established to evaluate the function of Sef. Briefly, Sef was inhaled before I/R operation. The levels of TIMP3, oxidative damage-related factors, and mitogen activated protein kinases (MAPKs) pathway-related factors were measured by qRT-PCR and western blot. Myocardial infarction (MI) area was detected by triphenyl tetrazolium chloride (TTC) staining assay.
Results
Sef preconditioning reduced MI area in myocardial I/R injury mice and upregulated TIMP3 expression in myocardial tissues of I/R mice. In addition, downregulation of TIMP3 reversed the alleviating effects of Sef pretreatment on myocardial oxidative damage and inhibited the effect of Sef pretreatment on MAPKs pathway activity.
Conclusion
Sef preconditioning ameliorated myocardial I/R injury by modulating MAPKs pathway activity via upregulating TIMP3.
