PAIN RELIEF

HA reduces the action of joint nociceptors, which provides pain reduction within the joint. Sensitized nociceptive terminals within the joint tissue are affected by HA concentration, reducing the pain response exhibited by these terminals .

HA analgesic effects have been shown to occur at mechanosensitive stretch-activated ion channels, where channel activity is significantly decreased upon HA binding . HMW HA was shown to decrease mechanical sensitivity of stretch-activated ion channels, which effectively blocked the pain response.

The expression of the inducible COX-2 enzyme, which plays a key role in arthritis-associated inflammation and pain, was significantly decreased by CS administration with chronic Joint pain . Similar results have been obtainedin invitrostudies carried out with human articular cartilage explants, whereby CS treatment suppressed IL-1b-induced inducible NO synthase, COX-2 and prostaglandin E (PGE)-2 gene expression. Moreover, similar data NF-kB in chondrocytes. The reduction in the expression and/or activity of these inflammatory molecules may explain the mechanisms bywhich CS potentially exerts its beneficial effect not only in the synovium but also on the articular cartilage and subchondral bone during arthritis.