The goal of pharmacological osteoarthritis (OA) treatments is to reduce pain and thus increase patient joint function and quality of life. Retigabine, a potent Kv7/M channel activator, shows analgesic efficacy in animal models of chronic inflammatory and neuropathic pain. We hypothesized that retigabine may also mitigate OA pain. To determine the effects of retigabine on pain behavior associated with monosodium iodoacetate (MIA)-induced OA.
The OA model was established with an intra-articular injection of MIA through the right patellar ligament, animals were treated with retigabine, and pain-related behaviors were assessed.
Retigabine significantly increased the mechanical threshold and prolonged the withdrawal latency of OA rats at 3-14 days. Retigabine also increased the mechanical threshold and prolonged the withdrawal latency of OA pain in a dose-dependent manner, with the strongest antinociceptive effect occurring at 60 min. The antinociceptive effects of retigabine were fully antagonized by the Kv7/M channel blocker XE991.
Retigabine showed antinociceptive effects for OA pain in the MIA model at different times during pain development. Retigabine may be an alternative therapeutic treatment for OA.