The Plasticity of Nanofibrous Matrix Regulates Fibroblast Activation in Fibrosis.

Natural extracellular matrix (ECM) mostly has a fibrous structure that supports and mechanically interacts with local residing cells to guide their behaviors. The effect of ECM elasticity on cell behaviors has been extensively investigated, while less attention has been paid to the effect of matrix fiber-network plasticity at microscale, although plastic remodeling of fibrous matrix is a common phenomenon in fibrosis. Here, a significant decrease is found in plasticity of native fibrotic tissues, which is associated with an increase in matrix crosslinking.

Integrated analysis of microRNA and mRNA expression profiles in rats with selenium deficiency and identification of associated miRNA-mRNA network.

Selenium deficiency is closely related with various type of cardiovascular disease. However, the miRNA-mRNA regulatory network in Selenium deficiency related cardiac change remains to be understand. In the present study, a reliable Selenium deficiency rat model was established and confirmed by pathological and biochemical examination.

Effects of extract from Ginkgo biloba on carbon tetrachloride-induced liver injury in rats.

Aim: To study the effects of extract from Ginkgo biloba (EGb) containing 22% flavonoid and 5% terpenoid on chronic liver injury and liver fibrosis of rats induced by carbon tetrachloride (CCl(4)).

Methods: All rats were randomly divided into control group, CCl(4)-treated group, colchicine-treated group and EGb-protected group. Chronic liver injury was induced in experimental groups by subcutaneous injection of CCl(4) and fed with chows premixed with 79.

Lovastatin reduces nuclear factor kappaB activation induced by C-reactive protein in human vascular endothelial cells.

The role of C-reactive protein (CRP) in atherogenesis has been supported by more recent data. Some studies have demonstrated marked up-regulation inflammatory responses in endothelial cells subjected to CRP. The nuclear factor-kappaB (NF-kappaB) signal transduction is known to play a key role in the expression of these proatherogenic entities.