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Electroacupuncture Ameliorates the Coronary Occlusion Related Tachycardia and Hypotension in Acute Rat Myocardial Ischemia Model: Potential Role of Hippocampus.

ABSTRACT: Mechanisms for electroacupuncture (EA) in disease treatments are still enigmatic. Here, we studied whether hippocampus was involved in the protection of EA stimulation on myocardial ischemia injury. Acute myocardial ischemia (AMI) model was produced. EA stimulation at heart meridian from Shenmen (HT7) to Tongli (HT5) was applied to rats 3 times a day for continuous three days. Coronary occlusion related tachycardia and hypotension, indicated by heart rate, mean arterial pressure, and rate pressure product, were apparently impaired after AMI injury. By contrast, EA stimulating could ameliorate the impairments of heart function (P < 0.05). Interestingly, lesion of CA1 region of hippocampus abolished the protection of EA. Neuronal activity in CA1 area was affected by AMI. As evidenced, cell counts, cell types, and frequency of the discharged neurons were facilitated after AMI, while EA stimulation attenuated the abnormalities. Furthermore, c-Fos expression was significantly facilitated in CA1 area after AMI, which was reduced by EA stimulation. Correlations were established between c-Fos expression and cell counts of discharged neurons, as well as between heart function and cell counts of discharged neurons. Taken together, EA stimulation at heart meridian protects against heart dysfunction induced by AMI possibly through suppressing the neuronal activity in CA1 region.

SUBMITTER: Wu S

PROVIDER: S-EPMC4499623 | biostudies-literature | 2015

REPOSITORIES: biostudies-literature

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Electroacupuncture Ameliorates the Coronary Occlusion Related Tachycardia and Hypotension in Acute Rat Myocardial Ischemia Model: Potential Role of Hippocampus.

Wu Shengbing S Cao Jian J Zhang Tianning T Zhou Yiping Y Wang Keming K Zhu Guoqi G Zhou Meiqi M

Evidence-based complementary and alternative medicine : eCAM 20150629

Mechanisms for electroacupuncture (EA) in disease treatments are still enigmatic. Here, we studied whether hippocampus was involved in the protection of EA stimulation on myocardial ischemia injury. Acute myocardial ischemia (AMI) model was produced. EA stimulation at heart meridian from Shenmen (HT7) to Tongli (HT5) was applied to rats 3 times a day for continuous three days. Coronary occlusion related tachycardia and hypotension, indicated by heart rate, mean arterial pressure, and rate pressu ...[more]

PMID: 26221181

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Project description:ObjectiveThe incidence of acute myocardial infarction (AMI) is increasing yearly. With the use of thrombolysis or percutaneous coronary intervention (PCI), the mortality rate of acute myocardial infarction has been significantly reduced. However, reperfusion can cause additional myocardial injury. There is still a lack of effective drugs to treat I/R injury, and it is urgent to find new therapeutic drugs.MethodsIn this study, network pharmacology was used to predict potential targets and biological processes involved in Muscone-mediated treatment of acute myocardial infarction. To model ischemia‒reperfusion injury, a hypoxia-reoxygenation model and in vivo ischemia‒reperfusion injury C57BL/6 mice model was constructed. Mice were treated with Muscone i.p. for 4 weeks. We detected the cardiac function on day 28.The expression levels of the apoptotic proteins Caspase-3 and Bax and the anti-apoptotic protein Bcl-2 were detected by immunoblotting after Muscone treatment of AC16 cells and in vivo. Additionally, the gene expression levels of the PUMA and p53 were analyzed by qRT‒PCR. Molecular docking was used to evaluate the binding energy between Muscone and NLRP3-related proteins. Immunoblotting and qRT‒PCR were used to assess the expression levels of NLRP3 signaling pathway-related proteins (NLRP3, ASC, and Caspase-1) and the NLRP3 gene, respectively. Moreover, the extracellular acidification rate of AC16 cells was measured using the Seahorse system to evaluate glycolysis levels after Muscone treatment. The expression of the key glycolytic enzyme PKM2 was analyzed by immunoblotting and qRT‒PCR. Finally, ChIP‒qPCR was performed to determine the levels of histone modifications (H3K4me3, H3K27me3, and H2AK119Ub) in the PKM2 promoter region.ResultsGO functional enrichment analysis revealed that muscone was involved in regulating the biological processes (BP) of AMI, which mainly included negative regulation of the apoptosis signaling pathway, the response to lipopolysaccharide, and blood pressure regulation. The cellular components (CC) involved in muscone-mediated regulation of AMI mainly included lipid rafts, membrane microdomains, and membrane regions. The molecular functions (MF) involved in muscone-mediated regulation of AMI mainly included oxidoreductase activity, nuclear receptor activity, and transcription factor activity. In vitro results indicated that muscone treatment could inhibit the expression levels of Bax and Caspase-3 in AC16 cells after ischemia‒reperfusion while increasing the expression level of the antiapoptotic protein Bcl-2. Muscone significantly suppressed the transcription levels of p53 and PUMA in AC16 cells. Molecular docking suggested that muscone could bind well with the Cryo-EM structure of NEK7(PDB ID:6NPY). Further investigation of inflammatory pathways revealed that muscone could inhibit the expression level of NLRP3 in AC16 cells and reduce the expression levels of Caspase-1 and Caspase recruitment domain. Fluorescent quantitative PCR experiments showed that muscone significantly inhibited the transcription of NLRP3. Moreover, we found that muscone could enhance the glycolytic efficiency of AC16 cells, which may be related to the increased protein expression of PKM2 in AC16 cells. Fluorescent quantitative PCR showed that muscone could increase the transcription level of PKM2. Chromatin immunoprecipitation assays showed that muscone treatment increased the expression level of H3K4me3 in the PKM2 promoter region and inhibited the levels of H3K27me3 and H2AK119Ub in the PKM2 promoter region.ConclusionMuscone promoted myocardial glycolysis and inhibited NLRP3 pathway activation to improve myocardial ischemia‒reperfusion injury.

Project description:It is unclear whether stable, high-risk patients with persistent total occlusion of the infarct-related coronary artery identified after the currently accepted period for myocardial salvage has passed should undergo percutaneous coronary intervention (PCI) in addition to receiving optimal medical therapy to reduce the risk of subsequent events.We conducted a randomized study involving 2166 stable patients who had total occlusion of the infarct-related artery 3 to 28 days after myocardial infarction and who met a high-risk criterion (an ejection fraction of <50% or proximal occlusion). Of these patients, 1082 were assigned to routine PCI and stenting with optimal medical therapy, and 1084 were assigned to optimal medical therapy alone. The primary end point was a composite of death, myocardial reinfarction, or New York Heart Association (NYHA) class IV heart failure.The 4-year cumulative primary event rate was 17.2% in the PCI group and 15.6% in the medical therapy group (hazard ratio for death, reinfarction, or heart failure in the PCI group as compared with the medical therapy group, 1.16; 95% confidence interval [CI], 0.92 to 1.45; P=0.20). Rates of myocardial reinfarction (fatal and nonfatal) were 7.0% and 5.3% in the two groups, respectively (hazard ratio, 1.36; 95% CI, 0.92 to 2.00; P=0.13). Rates of nonfatal reinfarction were 6.9% and 5.0%, respectively (hazard ratio, 1.44; 95% CI, 0.96 to 2.16; P=0.08); only six reinfarctions (0.6%) were related to assigned PCI procedures. Rates of NYHA class IV heart failure (4.4% vs. 4.5%) and death (9.1% vs. 9.4%) were similar. There was no interaction between treatment effect and any subgroup variable (age, sex, race or ethnic group, infarct-related artery, ejection fraction, diabetes, Killip class, and the time from myocardial infarction to randomization).PCI did not reduce the occurrence of death, reinfarction, or heart failure, and there was a trend toward excess reinfarction during 4 years of follow-up in stable patients with occlusion of the infarct-related artery 3 to 28 days after myocardial infarction. (ClinicalTrials.gov number, NCT00004562 [ClinicalTrials.gov].).

Dataset Information

Electroacupuncture Ameliorates the Coronary Occlusion Related Tachycardia and Hypotension in Acute Rat Myocardial Ischemia Model: Potential Role of Hippocampus.

Publications

Electroacupuncture Ameliorates the Coronary Occlusion Related Tachycardia and Hypotension in Acute Rat Myocardial Ischemia Model: Potential Role of Hippocampus.

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