TNFAIP3 alleviates pain in lumbar disc herniation rats by inhibiting the NF-κB pathway.

Background: It's been reported that the tumor necrosis factor alpha inducible protein 3 () gene played an important role in the pathogenesis of autoimmune and chronic inflammation diseases. Moreover, in degenerative diseases of the lumbar spine the nuclear factor-κB (NF-κB) pathway is significantly activated. This study aimed to explore the role of the tumor necrosis protein-induced zinc finger protein A20 (A20) protein in degenerative diseases of the lumbar spine on the NF-κBp65 pathway.

The Expression Levels and Significance of GSH, MDA, SOD, and 8-OHdG in Osteochondral Defects of Rabbit Knee Joints.

Objective: To observe the dynamic changes in oxidative stress and the expression levels of antioxidant and oxidative parameters in the blood and synovial fluid in the osteochondral defects of the rabbit knee joints and to explore the significance.

Methods: Thirty New Zealand white rabbits were randomly selected and divided into a blank control group ( = 10), a model control group ( = 10), and an osteochondral defect group ( = 10). The osteochondral defect model of rabbit knee joint was constructed by medial parapatellar arthrotomy.

Targeting NLRP3 inflammasome improved the neurogenesis and post-stroke cognition in a mouse model of photothrombotic stroke.

Post-stroke cognitive impairment (PSCI) severely affects the quality of a survivor's life, but its neurophysiological basis remains unknown. Neuroinflammation has been considered as an important contributor to PSCI, which could be induced or exacerbated by system inflammation. NACHT-LRR- and pyrin-domain-containing protein 3 (NLRP3) inflammasome is the most widely studied in the initiation of inflammation.

Highly sensitive determination of reduced glutathione based on a cobalt nanoparticle implanted-modified indium tin oxide electrode.

Cobalt nanoparticle modified indium tin oxide (CoNP/ITO) electrodes fabricated by ion implantation were applied for the detection of reduced glutathione (GSH). The CoNP/ITO electrode was characterized by scanning electron microscopy (SEM), energy dispersive X-ray (EDX) detector and X-ray photoelectron spectroscopy (XPS). The assay performance with regard to GSH were evaluated by cyclic voltammetry (CV) and chronoamperometry (I-t).

Venlafaxine modulates depression-induced behaviour and the expression of Bax mRNA and Bcl-xl mRNA in both hippocampus and myocardium.

Objectives: Major depressive disorder is associated with progressive brain changes and is frequently comorbid with cardiovascular disease. There may be shared pathophysiological pathways between cerebral and myocardial dysfunction that impact on apoptosis related proteins. Our aim was to examine behaviour changes of rats with chronic mild stress (CMS), explore the expression of Bax and Bcl-xl in the hippocampus and myocardium, and additionally evaluate the effects of venlafaxine on these molecular mechanisms.

Involvement of dimethylarginine dimethylaminohydrolase-2 in visfatin-enhanced angiogenic function of endothelial cells.

Background: Visfatin, a new adipocytokine, was reported to promote angiogenesis. Dimethylarginine dimethylaminohydrolase (DDAH), which could regulate vascular endothelial growth factor (VEGF) expression in endothelial cells, is thought as a novel modulator of angiogenesis. The aim of the study was to investigate the role of DDAH2 in visfatin-induced angiogenesis in human umbilical vein endothelial cells (HUVECs).