Efficacy of electroacupuncture pretreatment for myocardial injury in patients undergoing percutaneous coronary intervention: A randomized clinical trial with a 2-year follow-up.

Electroacupuncture pretreatment (EAP) safely protects the heart from ischemic injury, however, the efficacy of EAP for periprocedural myocardial injury after percutaneous coronary intervention (PCI) remains unclear. Our aim was to investigate whether EAP prior to PCI reduces post-PCI myocardial injury in patients with coronary artery disease (CAD). 388 patients (≥ 18 years old) with CAD, undergoing elective PCI were enrolled and randomized, out of those 204 went through the whole trial. EAP was conducted by 30-minute electrical stimulation through 4 electrodes attached to the Antiguan (PC6) and Ximen (PC4) acupoints in the forearm bilaterally 1-2h prior to PCI. The control group had sham electrodes but no electrical stimulation. The primary end point was the incidence of myocardial infarction type 4a (MI4a) based on serum cTnI values at 24h after PCI. The secondary end points included post-procedural cardiac function and the major adverse cardiac/cerebrovascular event (MACCE) rate. EAP prior to PCI significantly reduced the incidence of MI4a (serum cTnI≥0.20 ng/mL) 24h post-PCI compared to the control group (P=0.004). The echocardiography at 6 months after PCI revealed significant improvement in cardiac function in the EAP group compared with the control group. The MACCE rate was significantly decreased in the EAP group at 24 month follow-up compared to the control group (P=0.0157). Moreover, multivariate logistic regression analysis showed that EAP was associated with decreased likelihood of MACCE (odds ratio 0.327, 95% CI 0.140-0.767, P=0.010). EAP prior to PCI significantly reduced cTnI release and protected patients with CAD from subsequent myocardial injury after PCI procedure.

Calorie Restriction Attenuates Monocrotaline-induced Pulmonary Arterial Hypertension in Rats.

Calorie restriction (CR) is one of the most effective nonpharmacological interventions protecting against cardiovascular disease, such as hypertension in the systemic circulation. However, whether CR could attenuate pulmonary arterial hypertension (PAH) is largely unknown. The PAH model was developed by subjecting the rats to a single subcutaneous injection of monocrotaline. CR lowered mean pulmonary arterial pressure (mPAP) and reduced vascular remodeling and right ventricular hypertrophy in PAH rats. Meanwhile, CR attenuated endothelial dysfunction as evidenced by increased relaxation in response to acetylcholine. The beneficial effects of CR were associated with restored sirtuin-1 (SIRT1) expression and endothelial nitric oxide synthase (eNOS) phosphorylation and reduced eNOS acetylation in pulmonary arteries of PAH rats. To further clarify the role of SIRT1 in the protective effects of CR, adenoviral vectors for overexpression of SIRT1 were administered intratracheally at 1 day before monocrotaline injection. Overexpression of SIRT1 exhibited similar beneficial effects on mPAP and endothelial function, and increased eNOS phosphorylation and reduced eNOS acetylation in the absence of CR. Moreover, SIRT1 overexpression attenuated the increase in mPAP in hypoxia-induced PAH animals. Overall, the present data demonstrate that CR may serve as an effective treatment of PAH, and targeting the SIRT1/eNOS pathway may improve treatment of PAH.

Hypoxia inducible factor-1α expression is associated with hippocampal apoptosis during epileptogenesis.

Cell apoptosis can cause hippocampal neuronal loss after epileptic seizures. Hypoxia inducible factor (HIF)-1α is an important factor mediating apoptosis after brain injuries, such as cerebral ischemia and traumatic brain injures, but little research has been done on its role in the lithium chloride-pilocarpine induced epileptic model. Here, we used a rat model of pilocarpine-induced status epilepticus (SE) to investigate HIF-1α expression and apoptosis in the hippocampus, and to explore their relationship during epileptogenesis. 120 male Sprague Dawley (SD) rats were treated with lithium chloride-pilocarpine injections and divided into an experimental group (administered by MK-801) and a positive control group (administered by saline). Then the HIF-1α expression and hippocampal apoptosis were investigated by histological confirmation and western blotting at 24h, 3d, 7d and 14d, respectively. The results showed that the administration of MK-801 significantly reduced (P<0.05) HIF-1α expression and hippocampal apoptosis during epileptogenesis in comparison with the positive control. Moreover, the expression of HIF-1α and hippocampal apoptosis presented significant time-dependent changes (P<0.01) within 2 weeks, and their positive correlation (P<0.05) analyzed by Pearson׳s correlation analysis. Meanwhile, the HIF-1α immunostained cells were distributed in accord with TUNEL immunostained cells and Caspase-3 immunopositive cells in the hippocampus. These results indicate that the HIF-1α expression is associated with hippocampal apoptosis, and suggest that HIF-1α is an important factor during epileptogenesis.

Genetically engineered bone marrow mesenchymal stem cells improve functional outcome in a rat model of epilepsy.

Bone marrow mesenchymal stem cells (BMSCs) hold a great promising approach for the treatment of epilepsy owing to their distinctive characteristics and multi-potency. However, there is little research focusing on the multi-potency of BMSCs in the treatment of epilepsy, the present study was designed to examine the influence of genetically engineered BMSCs (GE-BMSCs) on the functional outcome in a rat model of epilepsy. First, Hes1 gene of BMSCs was genetically engineered by RNA interference (RNAi), and then the GABAergic differentiation of GE-BMSCs was tested in vitro. Second, the lithium chloride-pilocarpine induced epileptic rats were administrated with the GE-BMSCs, the behavioral observation and electroencephalography (EEG) monitoring was employed to analyze the functional outcome on the epileptic model at different time points (day 7, day 14, day 21 and day 28), followed by histological verification. In vitro test showed that Hes1 silencing could promote BMSCs to differentiate into GABAergic neuron-like cells. In vivo test showed that GE-BMSCs graft could further improve the functional recovery of the epileptic rats, and the GABAergic differentiation of grafted GE-BMSCs was correlated with the functional recovery. Taken together, these data suggest that GE-BMSCs can improve the functional outcome in a rat model of epilepsy.