Abstract
BackgroundHyperbaric oxygen (HBO) therapy is proven to attenuate neuropathic pain in rodents. The goal of the present study was to determine the potential involvement of the Kindlin-1/Wnt-10a signaling pathway during astrocyte activation and inflammation in a rodent model of neuropathic pain.MethodsRats were assigned into sham operation, chronic constriction injury (CCI), and CCI + HBO treatment groups. Neuropathic pain developed in rats following CCI of the sciatic nerve. Rats in the CCI + HBO group received HBO treatment for five consecutive days beginning on postoperative day 1. The mechanical withdrawal threshold (MWT) and the thermal withdrawal latency (TWL) tests were performed to determine mechanical and heat hypersensitivity of animals, respectively. Kindlin-1, Wnt-10a and β-catenin protein expression was examined by immunohistochemistry and Western blot analysis. Expression of tumor necrosis factor (TNF)-α was also determined by ELISA.ResultsOur findings demonstrated that HBO treatment significantly suppressed mechanical and thermal hypersensitivity in the CCI neuropathic pain model in rats. HBO therapy significantly reversed the up-regulation of Kindlin-1 in dorsal root ganglia (DRG), spinal cord, and hippocampus of CCI rats. CCI-induced astrocyte activation and increased levels of TNF-α were efficiently reversed by HBO (P < 0.05 vs. CCI). HBO also reversed Wnt-10a up-regulation induced by CCI in the DRG, spinal cord, and hippocampus (P < 0.05 vs. CCI).ConclusionsOur findings demonstrate that HBO attenuated CCI-induced rat neuropathic pain and inflammatory responses, possibly through regulation of the Kindlin-1/Wnt-10a signaling pathway.
Highlights
Hyperbaric oxygen (HBO) therapy is proven to attenuate neuropathic pain in rodents
Our results showed that HBO therapy attenuated neuropathic pain in rats, possibly through regulating Kindlin-1/Wnt-10a signaling, astrocyte activation, and subsequent inflammatory responses
mechanical withdrawal threshold (MWT) and thermal withdrawal latency (TWL) levels gradually decreased with time after surgery in animals of the constriction injury (CCI) group when compared with sham operation control rats (Fig. 1)
Summary
Hyperbaric oxygen (HBO) therapy is proven to attenuate neuropathic pain in rodents. The goal of the present study was to determine the potential involvement of the Kindlin-1/Wnt-10a signaling pathway during astrocyte activation and inflammation in a rodent model of neuropathic pain. Emerging lines of evidence suggest that HBO therapy can reduce chronic pain in animal models [9–11]. The use of HBO treatment has been proven to attenuate chronic cluster headaches and [12] idiopathic trigeminal neuralgia in patients [13]. Our previous study indicated that the antinociceptive effects of HBO therapy may be linked to inhibition of astrocyte activation and inflammation in a chronic constriction injury (CCI)-induced neuropathic pain model in rats [10]. The precise molecular mechanisms underpinning this process are currently unknown
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