BackgroundViral myocarditis, which is often caused by coxsackievirus B3 (CVB3), is a serious clinical disorder characterized by excessive myocardial inflammation. Valproic acid (VPA) is described as a histone deacetylase inhibitor that has anti-inflammatory effects in several inflammatory diseases. However, the role and the detailed mechanism of VPA in viral myocarditis remain unclear.MethodsExperimental CVB3-induced myocarditis was induced in mice by intraperitoneally (i.p.) infected with CVB3. VPA was i.p. administered from day 0 to day 7. The survival, body weight loss, and myocarditis severity of mice were recorded. Th17 and Treg cells in spleen were analyzed by flow cytometry. Th17/Treg cell-related cytokine expressions were quantified by ELISA. The effect of VPA on Th17 and Treg cells differentiation was examined in vitro and in vivo.ResultsAdministration of VPA significantly attenuated the clinical severity of myocarditis, and the overall mortality from CVB3-induced myocarditis. The infiltration of Th17 and Treg cells, as well as the serum level of related cytokines (IL-17A and IL-10), were increased in CVB3 infected mice. In addition, VPA decreased the percentage of splenic Th17 cells while increased the percentage of Treg cells. Moreover, VPA downregulated the expression of IL-17A and upregulated IL-10 in serum and heart tissues of CVB3 infected mice. Additionally, VPA directly inhibited the differentiation of Th17 cells and promoted both the differentiation and suppressive function of Treg cells in vitro and in vivo.ConclusionsOur results suggest that VPA may thus be a promising strategy in the therapy of viral myocarditis.

Power-quality analyzers are commonly used in power systems to estimate waveform distortion, including the parameters of harmonics/interharmonics. In our study, a calibration scheme was developed and verified. This scheme is capable of calibrating the interharmonics specification of power-quality analyzers under asynchronous sampling. In our scheme, the hardware structure is composed of an interharmonic signal source, a wide-frequency resistive voltage divider, a broadband current shunt, and a data acquisition system. A new algorithm, based on discrete Fourier transform and interpolation, is presented. The procedure is implemented by LabVIEW software to process the sampling data and obtain the final interharmonic parameters. The test results of the amplitudes of the interharmonic current and voltage indicate that the calibration accuracy is 3.0‰ (16 Hz–6 kHz) and 6.8‰ (6 kHz–9 kHz) for the voltage signal, and 3.5‰ (16 Hz–6 kHz) and 6.5‰ (6 kHz–9 kHz) for the current signal. This index is higher than that acquired by the recommended methods in the International Electrotechnical Commission (IEC) standard.

The aim of the present study was to investigate the effect of Lidocaine on hypoxia-induced injury in cardiomyoblasts whilst exploring the associated molecular mechanism. In the present study, hypoxia was induced in H9c2 cells to establish an in vitro model of myocardial infarction. The cells were treated with lidocaine (0.5, 1, 5, 10 mM) for 48 h under hypoxic conditions. Cell viability and apoptosis levels were determined by MTT assay and flow cytometry, and ELISA was used to measure the levels of inflammatory cytokines released. A creatine kinase isoenzyme/cardiac troponin I detection kit was used to show that lidocaine significantly reduced hypoxia-induced cardiac troponin 1 and creatine kinase-muscle/brain release in a dose-dependent manner. Mitochondrial viability staining suggested that lidocaine significantly enhanced mitochondrial viability under hypoxic conditions. Lidocaine also significantly reduced hypoxia-induced apoptosis and increased H9c2 viability in a dose-dependent manner. Additionally, under hypoxic conditions, lidocaine dose-dependently promoted Bcl-2 expression, while decreasing Bax and caspase-3 expression in H9c2 cells. ELISA and reverse transcription quantitative PCR were used to detect the levels of tumor necrosis factor (TNF-α), interleukin (IL)-1β and IL-6 released by H9c2 cells. Results showed that lidocaine markedly reduced the hypoxia-induced expression levels of IL-1β, TNF-α and IL-6 in a dose-dependent manner. In addition, protein levels of phosphorylated (p)-ERK1/2 and NF-κB p-p65 were analyzed by western blotting, and results indicated that lidocaine significantly increased the protein levels of p-ERK1/2 and decreased the protein level of NF-κB p-p65 in a dose-dependent manner under hypoxic conditions. These data suggested that lidocaine might protect cardiomyoblasts from hypoxia-induced injury via activation of the mitogen activated protein kinase/ERK/NF-κB signaling pathway.

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