Abstract
BackgroundHyperbaric oxygen (HBO) has the potential to relieve neuropathic pain. The purpose of this study was to determine whether the NO-cGMP-PKG signaling pathway is involved in the analgesic effects of early hyperbaric oxygen treatment of neuropathic pain in rats.MethodsRats were randomly grouped for establishment of chronic constriction injury (CCI) models. Intrathecal catheters were inserted and 2.5ATA HBO therapy was administered from day 1 post-surgery for 60 minutes daily, continuously for 5 days; menstruum NS, DMSO, NO synthase(NOS) nonspecific inhibitor (L-NAME), soluble guanylyl cyclase(sGC) inhibitor (ODQ) and protein kinase G(PKG) inhibitor (KT5823) were administered intrathecally 30 minutes prior to HBO therapy. Pain-related behaviors in rats were observed at specific time points. Western blot and real-time RT-PCR were used to observe the expressions of PKG1 mRNA and protein in the spinal dorsal horn.ResultsCompared with the CCI group, HBO could significantly relieve mechanical and thermal hyperalgesia in rats. After intrathecal administration of L-NAME, ODQ and KT5823, effects of HBO on relieving hyperalgesia in rats were reversed (P < 0.05 vs. HBO), and expression of PKG1 mRNA and protein decreased in the spinal dorsal horn of the animals (P < 0.05 vs. HBO).ConclusionsEarly HBO therapy could significantly improve symptoms of hyperalgesia of neuropathic pain in rats, possibly via activation of the NO-cGMP-PKG signaling transduction pathway.
Highlights
Hyperbaric oxygen (HBO) has the potential to relieve neuropathic pain
We found that HBO could significantly decrease the expression of inducible nitric oxide synthase (iNOS) and neuronal nitric oxide synthase (nNOS) in the spinal dorsal horn on the operative side, with no obvious change of endothelial nitric oxide synthase (eNOS) expression
Rats were numbered for surgeries of constriction injury (CCI) and intrathecal catheter insertion, and randomly divided into 7 groups: CCI group; HBO group; HBO + NS group (NS10μL); HBO + DMSO group (DMSO10μL); HBO + N-nitro-L-arginine methyl ester (L-NAME) group (L-NAME100μg/10 μL); HBO + ODQ group (ODQ10μg/10 μL); HBO + KT5823 group (KT5823 500 ng/10 μL). 2.5ATA hyperbaric oxygen therapy was performed from day 1 after surgery, for 60 minutes every day, continuously for 5 days; Menstruums and inhibitors were intrathecally administered 30 minutes prior to hyperbaric oxygen therapy
Summary
Hyperbaric oxygen (HBO) has the potential to relieve neuropathic pain. The purpose of this study was to determine whether the NO-cGMP-PKG signaling pathway is involved in the analgesic effects of early hyperbaric oxygen treatment of neuropathic pain in rats. International Association for the Study of Pain (IASP) [1] defined the neuropathic pain (NP) as pain induced by direct injury or dysfunction of the central or peripheral nervous systems. Hyperbaric oxygen (HBO) has a strong neuroprotective effect, and is widely used in the treatment of a variety of neurological diseases. Some advances in the treatment of chronic pain have been reported [5–7]. HBO has been reported to effectively relieve inflammatory pain [8]. Studies have reported that HBO could effectively relieve pain of two neuropathic pain models [9]. Previous studies noted that single HBO administration [10] could relieve mechanical allodynia
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