Why the study?
Sevoflurane preconditioning has been shown to relieve myocardial ischemia/reperfusion injury, but the underlying mechanisms remain unknown.
Does sevoflurane preconditioning alleviate myocardial ischemia/reperfusion injury in a mouse model?
Does sevoflurane preconditioning alleviate myocardial ischemia/reperfusion injury in a mouse model?
Sevoflurane preconditioning ameliorates myocardial ischemia/reperfusion injury in mice by upregulating TIMP3 and modulating MAPKs pathway activity.
Answers are grounded in this paper and cite their sources.
Does not support clinical use; leaves open TIMP3 as a target for human myocardial I/R 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.
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Wang et al. (2020) studied this question.
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