Emodin protects H9c2 cells from hypoxia-induced injury by up-regulating miR-138 expression.

Myocardial infarction (MI) is a common presentation for ischemic heart disease, which is a leading cause of death. Emodin is a Chinese herbal anthraquinone used in several diseases. However, the effect of emodin in hypoxia-induced injury in cardiomyocytes has not been clearly elucidated. Our study aimed to clarify the functions of emodin in hypoxia-induced injury in rat cardiomyocytes H9c2 and explore the underlying mechanism. The effects of emodin on cell viability and apoptosis were analyzed by the Cell counting kit-8 assay and flow cytometry assay, respectively. The cell proliferation- and cell apoptosis-related proteins were detected by western blot. qRT-PCR was used to determine the relative expression of miR-138. Cell transfection was performed to alter miR-138 and MLK3 expression. miR-138 target was performed by dual luciferase activity assay. Sirt1/AKT and Wnt/ß-catenin pathways-related factors phosphorylation were analyzed by western blot. Emodin inhibited hypoxia-induced injury in H9c2 cells by promoting cell viability and reducing cell apoptosis. miR-138 was down-regulated by hypoxia treatment but up-regulated by emodin. Up-regulation of miR-138 alleviated hypoxia-induced cell injury. Down-regulation of miR-138 attenuated the growth-promoting effect of emodin on hypoxia-induced injury, whereas up-regulation of miR-138 enhanced the growth-promoting effects of emodin. The underlying mechanism might be by inactivating Sirt1/AKT and Wnt/ß-catenin pathways. MLK3 was negatively regulated by miR-138 expression and inactivated Sirt1/AKT and Wnt/ß-catenin pathways. Emodin alleviated hypoxia-induced injury in H9c2 cells via up-regulation of miR-138 modulated by MLK3, as well as by activating Sirt1/AKT and Wnt/ß-catenin pathways.

Emodin protects H9c2 cells from hypoxia-induced injury by up-regulating miR-138 expression

Myocardial infarction (MI) is a common presentation for ischemic heart disease, which is a leading cause of death. Emodin is a Chinese herbal anthraquinone used in several diseases. However, the effect of emodin in hypoxia-induced injury in cardiomyocytes has not been clearly elucidated. Our study aimed to clarify the functions of emodin in hypoxia-induced injury in rat cardiomyocytes H9c2 and explore the underlying mechanism. The effects of emodin on cell viability and apoptosis were analyzed by the Cell counting kit-8 assay and flow cytometry assay, respectively. The cell proliferation- and cell apoptosis-related proteins were detected by western blot. qRT-PCR was used to determine the relative expression of miR-138. Cell transfection was performed to alter miR-138 and MLK3 expression. miR-138 target was performed by dual luciferase activity assay. Sirt1/AKT and Wnt/β-catenin pathways-related factors phosphorylation were analyzed by western blot. Emodin inhibited hypoxia-induced injury in H9c2 cells by promoting cell viability and reducing cell apoptosis. miR-138 was down-regulated by hypoxia treatment but up-regulated by emodin. Up-regulation of miR-138 alleviated hypoxia-induced cell injury. Down-regulation of miR-138 attenuated the growth-promoting effect of emodin on hypoxia-induced injury, whereas up-regulation of miR-138 enhanced the growth-promoting effects of emodin. The underlying mechanism might be by inactivating Sirt1/AKT and Wnt/β-catenin pathways. MLK3 was negatively regulated by miR-138 expression and inactivated Sirt1/AKT and Wnt/β-catenin pathways. Emodin alleviated hypoxia-induced injury in H9c2 cells via up-regulation of miR-138 modulated by MLK3, as well as by activating Sirt1/AKT and Wnt/β-catenin pathways.

Effects of aqueous extract of Arctium lappa L. roots on serum lipid metabolism.

Objective To identify potential genes that may be involved in lipid metabolism in rats after treatment with aqueous extract of Arctium lappa L (burdock). Methods Rats were randomly divided into six groups: (i) control (standard diet); (ii) model group (high-fat diet only); (iii) high-fat diet and low-dose aqueous burdock root extract (2 g/kg); (iv) high-fat diet and moderate-dose aqueous burdock root extract (4 g/kg); (v) high-fat diet and high-dose aqueous burdock root extract (8 g/kg); and (vi) a positive control group exposed to a high-fat diet and simvastatin (10 mg/kg). Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis was performed to find the potential candidate genes involved in the modulation of blood lipids by treatment with aqueous burdock root extract. Results Burdock root extract reduced body weight and cholesterol levels in rats. KEGG analysis revealed 113 genes that were involved in metabolic pathways. Of these, 27 potential genes associated with blood lipid metabolism were identified. Conclusions Aqueous extract of burdock root reduced body weight and cholesterol in rats, possibly by modulating the differential expression of genes.

Comparison of Direct Current Synchronized Cardioversion to Ibutilide-Guided Catheter Ablation for Long-Term Sinus Rhythm Maintenance After Isolated Pulmonary Vein Isolation of Persistent Atrial Fibrillation.

Use of the antiarrhythmic ibutilide after isolated pulmonary vein isolation (PVI) might distinguish atrial remodeling severity and cases requiring further substrate modification, thereby improving efficacy of persistent atrial fibrillation (AF) treatment. Ninety-six consecutive patients with persistent AF were randomized after PVI to either direct current synchronized cardioversion (DCC group, n = 48) or 1 mg of intravenous ibutilide (ibutilide group, n = 48) followed by no further intervention if AF converted to sinus rhythm (SR) within 30 minutes (ibutilide conversion subgroup) or by complex fractionated atrial electrogram (CFAE) ablation until SR recovery or complete CFAE elimination (ibutilide nonconversion subgroup). With similarly distributed baseline characteristics and no serious postablation complications, the primary end point of 12-month SR maintenance rate after PVI was significantly higher for ibutilide versus the DCC group before (75% vs 56%; p = 0.042) or after (83% vs 60%; p = 0.011) reablation at physician's discretion for recurrence beyond 3 months after PVI. After ibutilide administration, 21 of 48 patients (44%) converted to SR at 17 ± 8 minutes (mean ± SD); those in the ibutilide nonconversion subgroup had larger atrial size (47 ± 4 vs 45 ± 4; p = 0.025) and CFAE area (29 ± 8 vs 12 ± 5; p = 0.001) and longer AF duration (27 ± 6 vs 21 ± 10; p = 0.026). Among ibutilide conversion and nonconversion subgroups and DCC group, procedure, ablation, and x-ray exposure times differed significantly, as did 12-month SR maintenance rate before (81% vs 70% vs 56%; p = 0.043) or after reablation (86% vs 81% vs 60%; p = 0.042). In conclusion, in persistent AF treatment, ibutilide-guided ablation after PVI yields higher 1-year SR maintenance rate than PVI only.

Safety and efficacy of early radiofrequency catheter ablation in patients with paroxysmal atrial fibrillation complicated with amiodarone-induced thyrotoxicosis.

BACKGROUND: Amiodarone is an antiarrhythmic drug that is frequently used to control atrial fibrillation (AF). Many patients with AF are afraid of the risk of ablation and take amiodar-one, some patients develop amiodarone-induced thyrotoxicosis (AIT). The purpose of the study was to investigate the safety and efficacy of early radiofrequency catheter ablation in patients with paroxysmal AF complicated with AIT. METHODS: From the 146 consecutive patients with paroxysmal AF who had been treated with amiodarone and underwent 3-dimensional mapping system guided circumferential pulmonary vein isolation (PVI) at our center from January 2013 to June 2014, 20 had developed AIT. Thirty controls with normal thyroid function and matched for baseline characteristics were selected. RESULTS: Pulmonary vein isolation was completed in all patients without serious complications and with similar procedural (170.60 ± 14.80 vs. 158.18 ± 9.06 min; p = 0.062) and X-ray exposure (16.48 ± 2.15 vs. 15.36 ± 1.57 min; p = 0.058) time in AIT vs. control groups; however, upon coronary sinus catheter pacing (from 300 ms to 200 ms) after intrave-nous isoproterenol administration 30 min post PVI, rates of induction of AF (35% vs. 3.33%; p = 0.005) and of non-pulmonary vein-related atrial tachyarrhythmias (50% vs. 6.67%; p = 0.01) were higher, while those for atrial flutter (15% vs. 3.33%; p = 0.17) and atrial tachycardia (15% vs. 6.67%; p = 0.31) were similar, as was the recovery of conduction of pulmonary vein potential (15% vs. 30%; p = 0.191). In AIT vs. control group, atrial tachyarrhythmia recurrence rate was higher at 3 months (45% vs. 16.67%, p = 0.032) but not between 3 and 12 months (30% vs. 23.33%; p = 0.418) follow-up. CONCLUSIONS: Early catheter ablation for paroxysmal AF in patients with AIT appeared safe and effective albeit with higher atrial tachyarrhythmia recurrence rate up to 3 months but not beyond 12 months after PVI relative to controls.