Background: Central sensitization driven by glial activation-mediated
neuroinflammation is recognized as a key mechanism in
pain processing.
Laser moxibustion using low-intensity
laser irradiation of corresponding
acupoints significantly relieves
knee osteoarthritis (KOA)
pain. However, the underlying mechanism of its effects on KOA
pain is still not completely understood. Objective: In this study, we aimed to investigate whether
laser moxibustion could alleviate KOA
pain by inhibiting spinal glial activation and proinflammatory
cytokines upregulation in
monosodium iodoacetate (MIA)-induced KOA
pain in rats. Materials and methods: Sprague-Dawley rats were divided randomly into three groups: Saline +
Sham Laser, MIA +
Laser, and MIA +
Sham Laser.
A 10.6 μm
laser was used to irradiate ST35 (Dubi) for 10 min once every 2 days for a total of seven applications. The paw withdrawal mechanical threshold and weight-bearing distribution were performed to evaluate the nociceptive behaviors. Spinal expressions of microglial marker, ionized
calcium binding adaptor molecule-1 (Iba-1); astrocyte marker,
glial fibrillary acidic protein (GFAP); pro-inflammatory
cytokines,
tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and
interleukin-6 (IL-6) were measured 14 days after MIA injection. Results: The results showed that
laser moxibustion significantly reversed the MIA-induced
mechanical hyperalgesia and weight-bearing difference up to 14 days compared with MIA +
Sham Laser group (p < 0.05 or p < 0.01). Moreover, both the
protein level and immunofluorescence intensity of Iba-1 in the ipsilateral spinal cord dorsal horn were markedly decreased in the MIA +
Laser group than those in the MIA +
Sham Laser group (p < 0.01). However, there was no significant difference in the expression of GFAP between groups (p > 0.05). In addition,
laser moxibustion decreased the upregulation of TNF-α, IL-1β, and
IL-6 compared with the MIA +
Sham Laser group (p < 0.01). Conclusions: This study demonstrated that
laser moxibustion at ST35 significantly alleviated MIA-induced KOA
pain through inhibition of the microglial activation-mediated
neuroinflammation, at least partially, by suppressing the production of proinflammatory
cytokines, which may provide a potential
analgesic target for KOA
pain relief.