Objective <p>To observe the effect of pressing manipulation on pain sensitization of spinal cord dorsal horn (SCDH) in rats with myofascial trigger points.</p> Methods <p>Thirty-two male Sprague-Dawley rats were divided into a blank group (<i>n</i>=10) and a group for modeling (<i>n</i>=22) using the random number table method. Rats in the group for modeling were subjected to blunt blow plus centrifugal motion, and 20 rats successfully modeled were randomly divided into a model group and a pressing manipulation group, with 10 rats in each group. Rats in the blank group and the model group were reared routinely. Rats in the pressing manipulation group were subjected to pressing manipulation for 7.5 min continuously at 10 times/min, once every other day for a total of 7 times. After the values of pressure pain threshold (PPT) and soft tissue tension (STT) D<sub>0.2</sub> were measured in each group, the histomorphological changes at trigger points were observed. The expression levels of vesicular glutamate transporter 1 (VGluT1), M1 microglia marker (CD86), and M2 microglia marker (CD206) in lumbar enlargement’s SCDH were detected by immunohistochemistry. Western blotting was used to observe the expression levels of phosphorylated extracellular signal-regulated kinase 1/2 (p-ERK1/2), N-methyl-D-aspartic acid receptor 2B (NR2B), phosphorylated nuclear factor-kappa B p65 subunit (p-p65), interleukin (IL)-6, and tumor necrosis factor (TNF)-α.</p> Results <p>Compared with the blank group, the values of PPT and STT D<sub>0.2</sub> were significantly decreased (<i>P</i>&lt;0.05), and the morphological structure of muscle cells was changed with different sizes; the nucleus moved inward, inflammatory cells infiltrated between cells, and fibroblasts were increased in the model group. Compared with the model group, the values of PPT and STT D<sub>0.2</sub> were significantly higher (<i>P</i>&lt;0.05), the morphological structure of muscle cells showed improvement, and the phenomena of nuclear migration, inflammatory cell infiltration, and fibroblast proliferation were all reduced in the pressing manipulation group. Compared with the blank group, the expression levels of VGluTl, CD86, p-ERK1/2, NR2B, IL-6, TNF-α, and p-p65 were significantly increased (<i>P</i>&lt;0.05), and the expression level of CD206 was decreased (<i>P</i>&lt;0.05) in the lumbar enlargement’s SCDH in the model group. Following pressing manipulation intervention, the expression levels of the aforementioned proteins were significantly reduced (<i>P</i>&lt;0.05), while the expression level of CD206 was elevated (<i>P</i>&lt;0.05) in the lumbar enlargement’s SCDH in the pressing manipulation group.</p> Conclusion <p>The pressing manipulation in Tuina (Chinese therapeutic massage) may promote microglial polarization from M1 to M2 in lumbar enlargement’s SCDH in trigger point rats, reduce the release of inflammatory factors, and inhibit the activity of glutamate neurons and their synapses, thereby inhibiting pain sensitization and relieving pain.</p>

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Investigating the effect of pressing manipulation on pain sensitization of spinal cord dorsal horn in trigger point rats based on microglial polarization

  • Liya Tang,
  • Quanrui Jiang,
  • Jieling Pan,
  • Yuqiao Zhang,
  • Xiang Feng,
  • Kun Ai,
  • Wu Li,
  • Jiangshan Li

摘要

Objective

To observe the effect of pressing manipulation on pain sensitization of spinal cord dorsal horn (SCDH) in rats with myofascial trigger points.

Methods

Thirty-two male Sprague-Dawley rats were divided into a blank group (n=10) and a group for modeling (n=22) using the random number table method. Rats in the group for modeling were subjected to blunt blow plus centrifugal motion, and 20 rats successfully modeled were randomly divided into a model group and a pressing manipulation group, with 10 rats in each group. Rats in the blank group and the model group were reared routinely. Rats in the pressing manipulation group were subjected to pressing manipulation for 7.5 min continuously at 10 times/min, once every other day for a total of 7 times. After the values of pressure pain threshold (PPT) and soft tissue tension (STT) D0.2 were measured in each group, the histomorphological changes at trigger points were observed. The expression levels of vesicular glutamate transporter 1 (VGluT1), M1 microglia marker (CD86), and M2 microglia marker (CD206) in lumbar enlargement’s SCDH were detected by immunohistochemistry. Western blotting was used to observe the expression levels of phosphorylated extracellular signal-regulated kinase 1/2 (p-ERK1/2), N-methyl-D-aspartic acid receptor 2B (NR2B), phosphorylated nuclear factor-kappa B p65 subunit (p-p65), interleukin (IL)-6, and tumor necrosis factor (TNF)-α.

Results

Compared with the blank group, the values of PPT and STT D0.2 were significantly decreased (P<0.05), and the morphological structure of muscle cells was changed with different sizes; the nucleus moved inward, inflammatory cells infiltrated between cells, and fibroblasts were increased in the model group. Compared with the model group, the values of PPT and STT D0.2 were significantly higher (P<0.05), the morphological structure of muscle cells showed improvement, and the phenomena of nuclear migration, inflammatory cell infiltration, and fibroblast proliferation were all reduced in the pressing manipulation group. Compared with the blank group, the expression levels of VGluTl, CD86, p-ERK1/2, NR2B, IL-6, TNF-α, and p-p65 were significantly increased (P<0.05), and the expression level of CD206 was decreased (P<0.05) in the lumbar enlargement’s SCDH in the model group. Following pressing manipulation intervention, the expression levels of the aforementioned proteins were significantly reduced (P<0.05), while the expression level of CD206 was elevated (P<0.05) in the lumbar enlargement’s SCDH in the pressing manipulation group.

Conclusion

The pressing manipulation in Tuina (Chinese therapeutic massage) may promote microglial polarization from M1 to M2 in lumbar enlargement’s SCDH in trigger point rats, reduce the release of inflammatory factors, and inhibit the activity of glutamate neurons and their synapses, thereby inhibiting pain sensitization and relieving pain.