Overexpression of steroid receptor coactivators alleviates hyperglycemia-induced endothelial cell injury in rats through activating the PI3K/Akt pathway.

Hyperglycemia is a major factor in vascular endothelial injury that finally leads to a cardiovascular event. Steroid receptor coactivators (SRCs) are a group of non-DNA binding proteins that induce structural changes in steroid receptors (nuclear receptors) critical for transcriptional activation. SRCs, namely, SRC-1, SRC-2, and SRC-3, are implicated in the regulation of vascular homeostasis.

Differential neurometabolite alterations in brains of medication-free individuals with bipolar disorder and those with unipolar depression: a two-dimensional proton magnetic resonance spectroscopy study.

Objectives: Bipolar disorder (BD) is a mental disorder characterized by periods of elevated mood and depression. Many individuals with BD are initially misdiagnosed and treated for unipolar depression (UD). In this study, we report direct comparisons between medication-free individuals with BD and those with UD in terms of the neurometabolites in the anterior cingulate cortex (ACC), medial prefrontal cortex (mPFC), parietal cortex (PC), and posterior cingulate cortex (PCC) of the brain.

The anti-fibrotic effects of microRNA-153 by targeting TGFBR-2 in pulmonary fibrosis.

Idiopathic pulmonary fibrosis (IPF) is a progressive interstitial fibrotic lung disease with an undefined etiology and no effective treatments. By binding to cell surface receptors, transforming growth factor-β (TGF-β) plays a pivotal role in lung fibrosis. Therefore, the screening of microRNAs (miRNAs), especially those interrupting the effects of TGF-β, may provide information not only on the pathomechanism, but also on the treatment of this disease.

miR-29c regulates NAV3 protein expression in a transgenic mouse model of Alzheimer's disease.

The microRNA-29 family (miRNA-29s) has three mature members, miR-29a, miR-29b and miR-29c, which have been implicated in the regulation of the pathogenesis of Alzheimer's disease (AD). The miR-29 family members exhibit differential regulation in various diseases and different subcellular distribution. In the present study, we initially investigated differential expression of miR-29c in the hippocampus and the frontal cortex of the young APPswe/PSΔE9 mouse brain, accompanied by inverse expression of neurone navigator 3 (NAV3), a regulator of axon guidance.

Treatment with PPARδ agonist alleviates non-alcoholic fatty liver disease by modulating glucose and fatty acid metabolic enzymes in a rat model.

Non-alcoholic fatty liver disease (NAFLD) is an increasingly common condition which is associated with certain features of metabolic syndrome and insulin resistance. Peroxisome proliferator‑activated receptor (PPAR)δ is an important regulator of energy metabolism and insulin resistance in diabetes. However, the function of PPARδ in NAFLD has not yet been fully elucidated.

Melatonin inhibits tunicamycin-induced endoplasmic reticulum stress and insulin resistance in skeletal muscle cells.

The prevalence of type 2 diabetes mellitus (T2D) is increasing worldwide. Melatonin possesses various beneficial metabolic actions, decreased levels of which may accelerate T2D. Endoplasmic reticulum stress (ERS) has been linked to insulin resistance in multiple tissues, but the role of melatonin on ERS and insulin resistance in skeletal muscle has not yet been investigated.

TCF2 attenuates FFA-induced damage in islet β-cells by regulating production of insulin and ROS.

Free fatty acids (FFAs) are cytotoxic to pancreatic islet β-cells and play a crucial role in the diabetes disease process. A recent study revealed a down-regulation of transcription factor 2 (TCF2) levels during FFA-mediated cytotoxicity in pancreatic β-cells. However, its function during this process and the underlying mechanism remains unclear.

CCN5 overexpression inhibits profibrotic phenotypes via the PI3K/Akt signaling pathway in lung fibroblasts isolated from patients with idiopathic pulmonary fibrosis and in an in vivo model of lung fibrosis.

Idiopathic pulmonary fibrosis (IPF) is a chronic and progressive interstitial lung disease with unknown etiology and undefined treatment modality. Fibroblasts are regarded as the major cell type that mediates the onset and progression of lung fibrosis by secreting large amounts of extracellular matrix (ECM) proteins, such as connective tissue growth factor (CTGF/CCN2). Current knowledge confers a crucial role of CCN2 in lung fibrosis.

Upregulation of adenosine A2A receptors induced by atypical antipsychotics and its correlation with sensory gating in schizophrenia patients.

Sensory gating deficits have been found in patients with schizophrenia and their unaffected relatives. However, the underlying neurobiological mechanism of this deficit remains unclear. Pre-clinical studies have implicated adenosine in sensory gating deficits in schizophrenia.

MicroRNA-153 negatively regulates the expression of amyloid precursor protein and amyloid precursor-like protein 2.

Increased expression of the amyloid precursor protein (APP) is a crucial risk factor of Alzheimer's disease (AD). Amyloid precursor-like protein 2 (APLP2), a homologue of APP, is also suggested to participate in AD pathogenesis. Accumulating evidence suggest the regulatory role of microRNA on AD-related genes.

[Significance and effect of Glucosidorum Tripterygii tororum on expressions of Foxp3 in regulatory T cells in type 1 diabetic rat model].

Aim: To investigate the significance and effect of Glucosidorum Tripterygii tororum (GTT) on the expressions of Foxp3 in CD4(+)CD25(+) regulatory T cells (Tr) in type 1 diabetic rat model.

Methods: 48 rats were divided evenly into 3 groups by random. Diabetic model was developed by multiple low dose intraperitoneal injection of streptozotocin in group II, III, and group I was treated as normal control.