Background
Hyperbaric oxygen therapy is increasingly used in adjuvant therapies to treat neuropathic pain. However, the specific targets of hyperbaric oxygen treatment in neuropathic pain remain unclear. Recently, we found that hyperbaric oxygen therapy produces an antinociceptive response via the kindlin-1/wnt-10a signaling pathway in a chronic pain injury model in rats.
Conclusions
Our findings demonstrate that kindlin-1 is a key protein in the action of hyperbaric oxygen therapy in the treatment of neuropathic pain. Indeed, interference with kindlin-1 may be a drug target for reducing the neuroinflammatory responses of the glial population in neuropathic pain.
Methods
The rats received an intraperitoneal injection of AAV-FERMT1 or an adeno-associated virus control vector 20 days before the chronic constriction injury operation. During five consecutive days of hyperbaric oxygen treatment, mechanical withdrawal threshold and thermal withdrawal latency tests were performed. Then, kindlin-1 expression was examined by real-time polymerase chain reaction and Western blot analysis. Meanwhile, the activation of glial cells and the production of TNF-α, IL-1β, and fractalkine were also determined.
Results
Our findings demonstrated that hyperbaric oxygen therapy inhibited the chronic constriction injury–induced increase in kindlin-1 expression. Furthermore, overexpression of kindlin-1 reversed the antinociceptive effects of hyperbaric oxygen therapy. The observed hyperbaric oxygen–induced reductions in glial cell activation and neuroinflammation, as indicated by the production of TNF-α, IL-1β, and fractalkine, were also prominently diminished in the group with kindlin-1 overexpression. Conclusions: Our findings demonstrate that kindlin-1 is a key protein in the action of hyperbaric oxygen therapy in the treatment of neuropathic pain. Indeed, interference with kindlin-1 may be a drug target for reducing the neuroinflammatory responses of the glial population in neuropathic pain.