Anti-Inflammatory Effects of Schisandrin B on LPS-Stimulated BV2 Microglia via Activating PPAR-γ.

Schisandrin B (Sch B), a dibenzocyclooctadiene lignan isolated from Schisandra chinensis (Turcz.) Baill, has been shown to have anti-inflammatory effect. The purpose of this study was to evaluate the effect of Sch B on LPS-induced inflammation in microglia and to investigate the molecular targets of Sch B.

The ratio of Th17/Treg cells as a risk indicator in early acute respiratory distress syndrome.

Introduction: Recent studies have revealed that lung inflammation mediated by CD4+ T cells may contribute to the pathogenesis of acute respiratory distress syndrome (ARDS). The imbalance between CD4 + CD25 + Foxp3 + regulatory T (Treg) cells and T helper (Th)17 cells has been found in a number of different inflammation and autoimmune diseases, while the role of the Th17/Treg balance in ARDS remains largely unknown. The aim of this study was to investigate the Th17/Treg pattern and its impact on disease severity and outcomes in patients with ARDS.

β-catenin induces A549 alveolar epithelial cell mesenchymal transition during pulmonary fibrosis.

Idiopathic pulmonary fibrosis (IPF) is a fatal lung disease characterized by expansion of the fibroblast and myofibroblast population and extracellular matrix deposition. Although the pathogenic mechanisms of IPF remain to be fully elucidated, there is emerging evidence that fibroblasts and myofibroblasts may be derived partially from alveolar epithelial cells by epithelial‑mesenchymal transition (EMT). In the present study, A549 cells were treated with different concentrations of Wnt1 and the results indicated that the mRNA and protein expression levels of vimentin, α‑smooth muscle actin (α‑SMA) and collagen Ⅰ gradully increased and those of E‑cadherin gradully decreased in a concentration‑dependent manner.

Effect of the Wnt1/β-catenin signalling pathway on human embryonic pulmonary fibroblasts.

Idiopathic pulmonary fibrosis (IPF) is a fibrotic lung disease associated with a high rate of mortality, characterised by an accumulation of fibroblasts/myofibroblasts in the fibroblastic foci (FF) and by an excessive deposition of extracellular matrix (ECM) in the lung parenchyma. The pathogenesis of this fatal disorder remains unclear. Previous evidence suggests that myofibroblasts are key effectors of the deposition of ECM.

Inhibition of epithelial-mesenchymal transition in A549 cell by transfected Napsin A.

Background: Epithelial-mesenchymal transition is a cellular process characterized by the loss of cell adhesion, inhibition of E-cadherin expression, and increased cell mobility. Cells without Napsin A are susceptible to transition. Further studies are required to investigate whether this transition can be reversed by restoration of Napsin A.

[Effect of Napsin A transfection into type II alveolar epithelial cells on pulmonary fibrosis].

Objective: To study the in vitro effect and mechanism of Napsin A gene transfection into type II alveolar epithelial cells on pulmonary fibrosis.

Methods: A recombinant lentiviral plasmid PLJM1-Napsin A was constructed and transfected into human type II alveolar epithelial cell line A549. The model of pulmonary fibrosis was established by the in vitro stimulation of A549 cells by transforming growth factor beta-1 (TGF-β1).

[Therapeutic effects and mechanism of saikosaponin-d in mice with bleomycin-induced pulmonary fibrosis].

Objective: To study the therapeutic effects and mechanism of saikosaponin-d (SSd) in mice with bleomycin (BLM)-induced pulmonary fibrosis.

Methods: According to the random number table, 180 mice were randomly divided into 5 groups. Four groups were pulmonary fibrosis models.

[Human lamada-interferon expressed in BHK-21 cell line and its bioactivity].

Aim: To construct the eukaryotic expressing vector PCAGG -HuIFN-lambda1 and PCAGG-HuIFN-lambda2 and to study the biological activity of HuIFN-lambda1and HuIFN-lambda2.

Methods: The cDNA fragment encodding HuIFN-lambda1 and HuIFN-lambda2 was amplified from the total RNA extracted from virus-induced HeLa cells by RT-PCR. Then it was cloned into the eukaryotic expressing vector PCAGG-EGFP.

Effect of NaCl and Helicobacter pylori vacuolating cytotoxin on cytokine expression and viability.

Aim: To determine whether Helicobacter pylori (H pylori) vacuolating cytotoxin (VacA) regulates release of pro-inflammatory cytokines (IL-1beta, IL-8, TNF-alpha, and IL-6) or alters gastric epithelial cell viability and to determine whether NaCl affects these VacA-induced changes.

Methods: Vacuolating activity was determined by measuring the uptake of neutral red into vacuoles of VacA-treated human gastric epithelial (AGS) cells. AGS cell viability was assessed by direct cell counting.

[Detection of telomerase activity in bronchoscopic brush-off samples in patients with lung cancer].

Background And Objective: Recent studies have shown that activation of telomerase plays an important role in carcinogenesis. However, there was few report on the level of telomerase activity in small samples from the patients with lung cancer. This study was designed to investigate the diagnostic significance of the detection of telomerase activity in bronchoscopic brush-off cells from the patients with lung cancer.