[Progress on treatment for stenosing tenosynovitis].

Radial styloid stenosing tenosynovitis is a kind of common chronic motor system injuries, and could lead to joint pain and aggravates with activity, in further makes a great impact on people's daily life. At present, therapeutic methods for this disease could divid into conservative treatment and surgical treatment. What we pay attention to is cure. Conservative treatment could effectively relieve pain and improve wrist motion in acute phase, however, it make little difference on long--term effect and usually cause to reappear. Surgical treatment, as a kind of invasive therapies, is chosen only when facing recalcitrant radial styloid stenosing tenosynovitis with many complications for its high cure rate. The author thought that patient education should play an important role in the therapy of radial styloid stenosing tenosynovitis, comprehensive treatment could be applied according to the different conditions of disease development, and could increase cure disease.

Edaravone protects against oxygen-glucose-serum deprivation/restoration-induced apoptosis in spinal cord astrocytes by inhibiting integrated stress response.

We previously found that oxygen-glucose-serum deprivation/restoration (OGSD/R) induces apoptosis of spinal cord astrocytes, possibly via caspase-12 and the integrated stress response, which involves protein kinase R-like endoplasmic reticulum kinase (PERK), eukaryotic initiation factor 2-alpha (eIF2α) and activating transcription factor 4 (ATF4). We hypothesized that edaravone, a low molecular weight, lipophilic free radical scavenger, would reduce OGSD/R-induced apoptosis of spinal cord astrocytes. To test this, we established primary cultures of rat astrocytes, and exposed them to 8 hours/6 hours of OGSD/R with or without edaravone (0.1, 1, 10, 100 µM) treatment. We found that 100 µM of edaravone significantly suppressed astrocyte apoptosis and inhibited the release of reactive oxygen species. It also inhibited the activation of caspase-12 and caspase-3, and reduced the expression of homologous CCAAT/enhancer binding protein, phosphorylated (p)-PERK, p-eIF2α, and ATF4. These results point to a new use of an established drug in the prevention of OGSD/R-mediated spinal cord astrocyte apoptosis via the integrated stress response.