This study investigated whether electroacupuncture (EA) confers protection against myocardial ischemia-reperfusion injury (MIRI) in rats and sought to elucidate underlying molecular mechanisms using proteomic and metabolomic profiling. The authors applied EA at classical acupuncture points and combined physiologic, histologic, biochemical, and multi-omics readouts to assess therapeutic efficacy and molecular changes.
Forty male Sprague–Dawley rats were randomly assigned to four groups: sham, model (ischemia/reperfusion, I/R, also referred to as MI group in the abstract), I/R with EA applied at Neiguan (PC6) and Zusanli (ST36) (denoted ST36 group), and I/R with sham acupuncture (MI+sham group). The MIRI model was established by ligation of the left anterior descending coronary artery followed by reperfusion. The abstract identifies the number of animals and groups but does not provide further details on randomization methods, inclusion/exclusion criteria, or sample sizes per group beyond the total.
EA stimulation in the treatment group targeted PC6 (Neiguan) and ST36 (Zusanli). A sham-acupuncture procedure was applied in the MI+sham group to control for nonspecific effects of needling/manipulation. The abstract reports these procedural assignments but does not include parameters of EA (frequency, intensity, duration, timing relative to ischemia/reperfusion) or the exact technique for sham acupuncture; those details were not reported in the available abstract.
The study used a combination of functional, histological, biochemical, and omics techniques: transthoracic echocardiography to assess cardiac systolic function; Evans blue‑TTC double staining to quantify myocardial infarct size; enzyme-linked immunosorbent assays (ELISA) to measure circulating inflammatory cytokines; and proteomic and metabolomic analyses to characterize molecular alterations. These methods were applied to evaluate the therapeutic effect of EA and to identify candidate molecular pathways associated with protection.
Compared with the I/R model group, EA treatment markedly reduced myocardial infarct size as measured by Evans blue‑TTC staining. Echocardiography showed improved cardiac systolic function in EA-treated animals. The abstract presents these comparative outcomes but does not provide numeric values, statistical measures, or time points; such quantitative details were not reported in the abstract.
EA decreased systemic inflammatory mediators: serum levels of IL-6, IL-1, and TNF-α were lower after EA compared with the I/R model. In myocardial tissue, expression of high mobility group box 1 (HMGB1) was also reduced in the EA group. The abstract indicates these anti-inflammatory effects as part of the cardioprotective response but omits exact concentrations, fold changes, or statistical data in the available summary.
Differential proteomic analysis identified a total of 6,676 proteins. The abstract is truncated at the point where further proteomic results would be described; therefore, specific differentially expressed proteins, pathway enrichment results, or quantitative changes were not available in the provided text. The identification of this large proteome suggests extensive characterization, but details of sample preparation, instrumentation, thresholds for differential expression, and key protein-level findings were not reported in the accessible abstract.
The authors indicate use of metabolomic techniques alongside proteomics to analyze molecular characteristics of EA treatment in MIRI. The abstract does not include the number of metabolites detected, major metabolic pathways altered, or specific metabolite changes, and these metabolomic results were not provided in the truncated abstract.
The abstract reports key experimental design elements and high-level outcomes but is truncated before completion of the proteomic description and does not report many quantitative details. Missing information in the available abstract includes EA stimulation parameters (frequency, intensity, duration, timing), exact group sample sizes, numeric outcome data with statistical testing, lists of differentially expressed proteins or metabolites, pathway analyses, and methods specifics for the multi-omics workflows. These details appear to be present in the full article but were not reported in the PubMed abstract excerpt.
In this rat MIRI model, EA at PC6 and ST36 was associated with reduced infarct size, improved systolic function, and diminished systemic and myocardial inflammation, including lower serum IL-6, IL-1, TNF-α, and reduced myocardial HMGB1 expression. Multi-omics profiling was performed and identified 6,676 proteins in the proteomic dataset, but full proteomic and metabolomic results and methodological specifics were not included in the available abstract. The reported findings support that EA modulates inflammatory and molecular responses in MIRI; readers interested in detailed omics results and procedural parameters should consult the full text.