Key result
Electroacupuncture pretreatment reduces myocardial infarct size ~14 percentage points vs ischemia-reperfusion in mice.
Why the study?
Does electroacupuncture pretreatment reduce myocardial ischemia-reperfusion injury and inflammatory responses by inhibiting Egr-1 expression via the ERK1/2 pathway in mice?
Does electroacupuncture pretreatment reduce myocardial ischemia-reperfusion injury and inflammatory responses by inhibiting Egr-1 expression via the ERK1/2 pathway in mice?
This preclinical study demonstrates that electroacupuncture at PC6 acupoints attenuates myocardial ischemia-reperfusion injury and inflammation in mice, mediated at least in part by inhibition of the ERK1/2-Egr-1 signaling pathway.
Answers are grounded in this paper and cite their sources.
Electroacupuncture may protect against ischemia-reperfusion injury in mice; leaves open clinical translation and requires human trials.
Early growth response- (Egr-) 1 is an upstream master switch in controlling inflammatory responses following myocardial ischemia-reperfusion (I/R). Activation of extracellular signal-regulated protein kinase-1 and kinase-2 (ERK1/2) signaling is known to upregulate Egr-1. ERK1/2 pathway has been previously shown to mediate the therapeutic action of electroacupucture (EA). Thus, we hypothesized that EA would reduce myocardial I/R injury and inflammatory responses through inhibiting Egr-1 expression via the ERK1/2 pathway. Mice were pretreated with EA, U0126, or combination of EA and U0126 and then underwent 1 h myocardial ischemia and 3 h reperfusion. We investigated that EA significantly attenuated the I/R-induced upregulation of both Egr-1 and phosporylated-ERK1/2 (p-ERK1/2), decreased myocardial inflammatory cytokines including tumor necrosis factor- α (TNF- α ) and interleukin-1 β (IL-1 β ), and reduced the infarct size and the release of cardiac troponin I (cTnI). U0126 treatment also exhibited the same effect as EA on Egr-1 level and subsequent cardioprotective effects. There was no additive effect of cotreatment with EA and U0126 on the expression of Egr-1 and its downstream target genes (TNF- α , IL-1 β ) or serum cTnI level. Collectively, these observations suggested that EA attenuates myocardial I/R injury, possibly through inhibiting the ERK1/2-Egr-1 signaling pathway and reducing the release of proinflammatory cytokines.
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Zhang et al. (2014) studied Myocardial ischemia-reperfusion injury (mouse model) (n=153). Electroacupuncture at bilateral PC6 acupoints (with or without U0126) vs. Ischemia-reperfusion alone, sham surgery, or vehicle control (0.1% v/v DMSO) was evaluated on Myocardial infarct size (ratio of infarct area to area at risk, IA/AAR) at 24 hours after reperfusion (p=0.019). Electroacupuncture pretreatment significantly reduced myocardial infarct size (IA/AAR) compared to ischemia-reperfusion alone (28.15% vs 42.64%, P=0.019) in mice.
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