The glucocorticoid dexamethasone alleviates allergic inflammation through a mitogen-activated protein kinase phosphatase-1-dependent mechanism in mice.

Glucocorticoids are widely used in the treatment of allergic and inflammatory diseases. Glucocorticoids have a widespread action on gene expression resulting in their pharmacological actions and also an array of adverse effects which limit their clinical use. It remains, however, to be studied which target gene effects are essential for the anti-allergic activity of glucocorticoids.

Electrospun decellularized extracellular matrix scaffolds promote the regeneration of injured neurons.

Traumatic injury to the spinal cord (SCI) causes the transection of neurons, formation of a lesion cavity, and remodeling of the microenvironment by excessive extracellular matrix (ECM) deposition and scar formation leading to a regeneration-prohibiting environment. Electrospun fiber scaffolds have been shown to simulate the ECM and increase neural alignment and neurite outgrowth contributing to a growth-permissive matrix. In this work, electrospun ECM-like fibers providing biochemical and topological cues are implemented into a scaffold to represent an oriented biomaterial suitable for the alignment and migration of neural cells in order to improve spinal cord regeneration.

Dexamethasone Attenuates the Expression of MMP-13 in Chondrocytes through MKP-1.

Mitogen-activated protein kinase phosphatase-1 (MKP-1) is upregulated in inflammation and reduces the activity of proinflammatory mitogen-activated protein kinases (MAP kinases) by dephosphorylation. MAP kinases are intracellular signaling pathways that mediate the cellular effects of proinflammatory cytokines. In the present study, we investigated the effects of the glucocorticoid dexamethasone on the expression of catabolic enzymes in chondrocytes and tested the hypothesis that these effects are mediated through MKP-1.

Pretreatment resistin levels are associated with erosive disease in early rheumatoid arthritis treated with disease-modifying anti-rheumatic drugs and infliximab.

Objective: Resistin is an adipocytokine related to insulin resistance and inflammation. We investigated whether resistin is associated with disease activity and inflammation in disease-modifying anti-rheumatic drug (DMARD)-naïve rheumatoid arthritis (RA) patients, whether it has predictive value for radiological disease progression, and whether tumour necrosis factor-α (TNF-α) is involved in these effects.

Method: Ninety-nine patients with early, DMARD-naïve RA participated in the NEO-RACo study.