[Analysis of DSG2, TTN and GATA4 gene variants in patients with Brugada syndrome from Henan].

OBJECTIVE: To explore the correlation between DSG2, TTN and GATA4 genes and Brugada syndrome in Henan Province of China. METHODS: From February 2017 to February 2019, 100 patients with Brugada syndrome and 100 healthy individuals were selected as the study and the control groups, respectively. Electrocardiogram and echocardiography were carried out, and peripheral blood samples was collected. Coding regions of DSG2, TTN and GATA4 genes were amplified by PCR and sequenced. The results were compared with standard sequences from GenBank. RESULTS: Electrocardiogram showed that all patients from the study group had ventricular arrhythmia, 87 cases (87%) presented ventricular tachycardia (VT), 84 cases (84%) presented T wave inversion, and 51 cases (51%) presented Epsilon wave. Echocardiography showed that the right ventricle in the study group was enlarged with the inner diameter of the right ventricle being (40.0±13.3) mm, and the right ventricle showed various degree of abnormal systolic function. The enlargement of right atrium accounted for 64%, and the involvement of the left ventricle accounted for 27%. The right ventricular diameter and left ventricular diastolic diameter of the study group were significantly greater than those of the control group (P< 0.05). DNA sequencing showed that 60 patients carried DSG2 gene variants, among which 18 had missense variant of exon 8. Fifty patients carried TTN gene variants, including 8 in the A-band domain and 3 in the I-band domain. Twenty patients carried 3 variants of the GATA4 gene. CONCLUSION: Variants of the DSG2, TTN and GATA4 genes in Henan region are correlated with the onset of Brugada syndrome.

Benzothiazole Treatment Regulates the Reactive Oxygen Species Metabolism and Phenylpropanoid Pathway of Rosa roxburghii Fruit to Delay Senescence During Low Temperature Storage.

Rosa roxburghii fruit were used as research objects to study the effects of different concentrations of benzothiazole (BTH) treatment on quality parameters, reactive oxygen species (ROS) metabolism, and the phenylpropanoid pathway during storage at 4°C for 14days. Results showed that BTH effectively delayed senescence with lower decay incidence, weight loss, and lipid peroxidation level and maintained the quality with higher contents of total soluble solid (TSS) content, titratable acidity (TA) in R. roxburghii fruit. Moreover, BTH increased hydrogen peroxide (H2O2) content, superoxide anion (O2 •-) production rate, and the activities and expression of superoxide dismutase (SOD), catalase (CAT), ascorbate peroxidase (APX), glutathione (GSH) reductase (GR), monodehydroascorbate reductase (MDHAR), dehydroascorbate reductase (DHAR), and peroxidase (POD), and the contents of GSH and ascorbic acid (AsA), but reduced the oxidized GSH (GSSG) content. In addition, the activities and gene expression of phenylalanine ammonia lyase (PAL), cinnamate 4-hydroxylase (C4H), and 4-coumarate-CoA ligase (4CL) and the concentrations of flavonoids, total phenols, and lignin were significantly elevated by BTH. These findings imply that BTH can delay senescence and maintain the quality of R. roxburghii fruit by modulating ROS metabolism and the phenylpropanoid pathway under low-temperature conditions.

MicroRNA-29b-3p Targets SPARC Gene to Protect Cardiocytes against Autophagy and Apoptosis in Hypoxic-Induced H9c2 Cells.

MicroRNAs participate in the regulation of abnormal cardiomyocyte apoptosis and autophagy, which leads to heart failure (HF). Lower miR-29b-3p levels were found in HF patients in this study. However, the role of miR-29b-3p in the molecular pathogenesis of HF remains unclear. Hypoxia-stimulated H9c2 cells were used an in vitro model of HF. It was found that hypoxia stimulation decreased the miR-29b-3p expression and enhanced cell apoptosis and autophagy response in H9c2 cells. While the effects of hypoxia on cell apoptosis and autophagy were reversed by miR-29b-3p transfection, especially 100 nM. The secreted protein acidic and rich in cysteine (SPARC), predicted as a direct target of miR-29b-3p, aggravated the hypoxia-induced cells apoptosis, autophagy, and TGFß1/Smad3 activation. While the changes were dramatically reversed by miR-29b-3p. Taken together, our data suggest that miR-29b-3p plays an important role in the progression of HF through targeting SPARC and regulating TGFß1/Smad3 pathway.