Nitric oxide-scavenging hyaluronic acid nanoparticles for osteoarthritis treatment.

Osteoarthritis (OA) is a degenerative arthritis disease marked by inflammation, pain, and cartilage deterioration. Elevated nitric oxide (NO) levels play a pivotal role in mediating OA-related inflammation and are found in abundance within OA joints. This study introduces a NO-scavenging hyaluronic acid conjugate (HA-NSc) bearing both lubrication and anti-inflammatory properties for the treatment of osteoarthritis.

Intracrystalline structure and physicochemical properties of mixed SiO2-TiO2 sol-pillared aluminosilicate.

Highly porous layered inorganic-inorganic nanohybrids were prepared by pillaring SiO2-TiO2 nanosol particles with aluminosilicate layers. According to powder X-ray diffraction analysis, the basal spacing of SiO2-TiO2 pillared aluminosilicate (STPC) calcined at 400 degrees C was determined to be larger than 40 A. N2 adsorption-desorption isotherm measurements showed the STPC to have a large Brunauer-Emmett-Teller surface area of approximately 590 m2/g, of which approximately 70% originates from micropores with a size range of 8-16 A.

Non-steroidal anti-inflammatory drugs inhibit nitric oxide-induced apoptosis and dedifferentiation of articular chondrocytes independent of cyclooxygenase activity.

Nitric oxide (NO) causes apoptosis and dedifferentiation of articular chondrocytes by the modulation of extracellular signal-regulated kinase (ERK), p38 kinase, and protein kinase C (PKC) alpha and -zeta. In this study, we investigated the effects and mechanisms of non-steroidal anti-inflammatory drugs (NSAIDs), such as indomethacin, ketoprofen, ibuprofen, sulindac sulfide, and flurbiprofen, in NO-induced apoptosis and dedifferentiation of articular chondrocytes. We found that all of the examined NSAIDs inhibited apoptosis and dedifferentiation.