As a common
joint disease,
osteoarthritis (OA) is often associated with
chronic pain. Synovial
inflammation is correlated with OA progression and
pain. Synovial
inflammation can produce a series of destructive substances, such as inflammatory factors and
pain mediators, which aggravate cartilage injury and further accelerate the progression of OA. Although many studies investigated the effects of synovial
inflammation on the onset and progression of OA, there are limited reports regarding slowing the progression of OA and relieving
pain by modulating synovial
inflammation. Therefore, there is an urgent need to search for safe and effective drugs to alleviate synovial
inflammation.
Dexmedetomidine, a selective α2 agonist, has been shown to have anti-inflammatory and
analgesic effects. However, its role and mechanism in OA remain unclear. Here, the effects and mechanisms of
dexmedetomidine in OA synovial
inflammation were investigated both in vivo and in vitro. We observed that
dexmedetomidine stunted LPS-induced migration and invasion of FLSs and the expression of inflammatory factors by upregulating
cannabinoid receptor type 2 (CB2) expression. Surprisingly, the application of
AM630 (CB2 antagonist) reversed this
therapeutic effect. The results of the animal experiments showed that
dexmedetomidine reduced synovial
inflammation and increased the pain threshold in an OA rat model. These preliminary results imply that
dexmedetomidine may be an effective compound for OA treatment.