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The present study integrated microRNA (miRNA) and mRNA expression data obtained from atrial fibrillation (AF) tissues and healthy tissues, in order to identify miRNAs and target genes that may be important in the development of AF. The GSE28954 miRNA expression profile and GSE2240 mRNA gene expression profile were downloaded from the Gene Expression Omnibus. Differentially expressed miRNAs and genes (DEGs) in AF tissues, compared with in control samples, were identified and hierarchically clustered. Subsequently, differentially expressed miRNAs and DEGs were searched for in the miRecords database and TarBase, and were used to construct a regulatory network using Cytoscape. Finally, functional analysis of the miRNA-targeted genes was conducted. After data processing, 71 differentially expressed miRNAs and 390 DEGs were identified between AF and normal tissues. A total of 3,506 miRNA-mRNA pairs were selected, of which 372 were simultaneously predicted by both miRecords and TarBase, and were therefore used to construct the miRNA-mRNA regulatory network. Furthermore, 10 miRNAs and 12 targeted mRNAs were detected, which formed 14 interactive pairs. The miRNA-targeted genes were significantly enriched into 14 Gene Ontology (GO) categories, of which the most significant was gene expression regulation (GO 10468), which was associated with 7 miRNAs and 8 target genes. These results suggest that the screened miRNAs and target genes may be target molecules in AF development, and may be beneficial for the early diagnosis and future treatment of AF. [ABSTRACT FROM AUTHOR]

The present study aimed to examine the status and clinical significance of cluster of differentiation (CD) 19+CD24highCD38high regulatory B cells (Bregs), serum interleukin (IL)‑10, serum transforming growth factor (TGF)‑β and IL‑10 receptor (IL‑10R) expression in peripheral blood from patients with systemic lupus erythematosus (SLE). A total of 56 patients with SLE and 35 healthy individuals were recruited to the present study. The SLE disease activity index (SLEDAI) was calculated, and other laboratory parameters were measured. Peripheral blood was collected from all participants. The frequency of CD19+CD24highCD38high Bregs and IL‑10R+ expression on circulating lymphocytes was examined by flow cytometry. The serum levels of IL‑10 and TGF‑β were measured using enzyme‑linked immunosorbent assay. The associations between these measurements and SLEDAI or other laboratory parameters were analyzed by correlation analysis. The percentage of CD19+CD24highCD38high Bregs and the serum levels of IL‑10 were significantly increased, whereas the expression of IL‑10R on circulating lymphocytes was markedly reduced in patients with SLE compared with in healthy controls. The serum levels of TGF‑β1 were not markedly different between the groups. In addition, these factors were correlated with other SLE laboratory parameters, and inter‑correlations were presented with different degrees of significance. The percentage of CD19+CD24highCD38high Bregs was positively correlated with the percentage of IL‑10R+ lymphocytes, mean fluorescence intensity (MFI) of IL‑10R+ lymphocytes and serum IL‑10 levels. In addition, the percentage of IL‑10R+ lymphocytes was positively correlated with its expression level (MFI), whereas serum TGF‑β1 levels were negatively correlated with serum IL‑10 levels. The present results indicated that expansion of CD19+CD24highCD38high Bregs, upregulation of IL‑10 and deficient lymphocyte‑associated IL‑10R may serve as novel SLE biomarkers. It may be hypothesized that deficient IL‑10R expression results in compensatory enhanced IL‑10 expression, expansion of Bregs, and/or compromised Breg and IL‑10 functions, thus contributing to SLE development. Therefore, targeting the ‘Bregs/IL‑10/IL‑10R’ system may provide a novel therapeutic approach for the treatment of SLE. [ABSTRACT FROM AUTHOR]

Baicalein (BA), one of the major bioactive flavonoids isolated from Scutellariae Radix, possesses various pharmacological activities. The present study aimed to investigate the protective effects of BA on tert-butyl hydroperoxide (t-BHP)-induced hepatotoxicity, and to investigate the potential mechanisms in LO2 cells. BA was demonstrated to possess protective properties against t-BHP injury in LO2 cells, as evidenced by MTT and lactate dehydrogenase assays. BA significantly prevented t-BHP-induced depolarization of mitochondrial membrane potential (MMP), decreased the percentage of apoptotic cells caused by t-BHP, and prevented intracellular reactive oxygen species (ROS) generation in LO2 cells. Furthermore, BA slightly triggered autophagy in LO2 cells, as evidenced by the elevation of LC3-II expression, while BA combined treatment with an autophagy inhibitor (chloroquine) or activator (rapamycin) did not alter the hepatoprotective properties. In conclusion, BA may possess a hepatoprotective effect against t-BHP-induced liver cell injury, dependent on ROS removal. Therefore, BA may represent a potential drug candidate in protecting hepatotoxicity. [ABSTRACT FROM AUTHOR]

Renal fibrosis is the final common pathway of all progressive renal disease. Excessive and chronic activation of the Wnt/β‑catenin signaling pathway results in chronic kidney disease (CKD) progression. To mimic CKD, the present study used 5/6‑nephrectomized rats, and alterations in kidney histology, expression of β‑catenin and renal cell apoptosis were assessed. In addition, mesangial cells were cultured in vitro and transfected with β‑catenin siRNA to evaluate the effect of blocking Wnt/β‑catenin signaling on cell apoptosis and the expression of markers of renal fibrosis. The results demonstrated that CKD rat kidney tissues exhibited moderate renal fibrosis and significantly increased expression levels of β‑catenin and apoptosis associated proteins compared with sham‑operated rats. In vitro, silencing of β‑catenin by siRNA attenuated tumor necrosis factor‑α‑induced apoptosis and decreased mRNA expression levels of various markers of fibrosis, including fibronectin, transforming growth factor‑β, and collagen I, III and IV. In conclusion, inhibition of Wnt/β‑catenin signaling by β‑catenin silencing attenuated apoptosis and expression of fibrosis‑associated markers in renal cells. The present study suggested that the Wnt/β‑catenin signaling pathway may serve as a potential treatment strategy for renal fibrotic disorders. [ABSTRACT FROM AUTHOR]

The aim of the present study was to report on a family with pathologically and genetically diagnosed autosomal dominant inherited centronuclear myopathy (CNM). In addition, this study aimed to investigate the clinical, pathological and molecular genetic characteristics of the disease. This pedigree was traced back three generations, four patients underwent neurological examination, two patients underwent muscle biopsy, and eight family members were subjected to dynamin 2 (DNM2) gene mutation analysis. DNM2 mutations were detected in seven family members, of which four patients exhibited DNM2 mutation-specific clinical and pathological features. Lower extremity weakness was the predominant symptom of these patients, however, proximal and distal lower extremity involvement was inconsistent. All patients exhibited marked systematic muscle atrophy and various degrees of facial muscle involvement. The patients presented the typical pathological changes of CNM, and their muscle tissues were heavily replaced by adipose tissue, with clustered distribution of muscle fibers as another notable feature. DNM2-CNM patients of this pedigree exhibited heterogeneous clinical and pathological features, providing a basis for further molecular genetic analysis. [ABSTRACT FROM AUTHOR]