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Rheumatoid arthritis (RA) is a chronic, etiology of inflammatory synovitis-based systemic disease. It is characterized by hand, small joints of the joints, symmetry, invasive joint inflammation, often associated with external organ involvement and serum rheumatoid factor positive, can lead to joint deformity and loss of function. At present, its main treatment program is to reduce the symptoms of RA and patients with signs, still lack of radical treatment of RA. Tumor necrosis factor (TNF) inhibition plays a dramatic role in the treatment of rheumatoid arthritis (RA) and have led to “congenital” more comprehensive evaluation of the immune system.
HMGB1, which was initially identified as part of the septic shock response and was recently rediscovered as a new proinflammatory cytokine. The levels of HMGB1 in sera and synovial fluid of RA patients were significantly higher in RA patients. The highest level of serum HMGB1 was found in early stage of RA. HMGB1 can also be induced by intra-articular injection of mice. Application of HMGB1 monoclonal antibody can reduce the severity of collagen-induced arthritis in mice.
These abnormal expressions of HMGB1 through a variety of molecular mechanisms in the pathogenesis of arthritis in several links to play a role in mediating the persistence of chronic inflammation and local tissue erosion damage. Blocking and inhibiting the role of HMGB1 can significantly reduce and improve Arthritis symptoms. This provides a new idea for elucidating the pathogenesis of RA and provides a new target for the treatment of RA.
YinY, LiW, DengM, et al. Extracellular high mobility group box chromosomal protein 1 promotes drug resistance by increasing the expression of Pglycoprotein expression in gastric adenocarcinoma cells. Mol Med Rep, 2014, 9(4):1439–1443.
In this study, the effect of extracellular release of HMGB1 by tumor cells on the expression of the chemotherapy resistance-related transporter proteins was analyzed in gastric adenocarcinoma cells. In addition, the effects of HMGB1 on resistance to anticancer drugs was determined.
Figure. Comparative computed tomography was used to determine the effect of various concentrations of HMGB1 on the expression of MDR1 in gastric adenocarcinoma cells.