Objective:

2

To illustrate the role of dehydrocorydaline (DHC) in chronic constriction injury (CCI)-induced neuropathic pain and the underlying mechanism.

Methods:

2

C57BL/6J mice were randomly divided into 3 groups by using a random number table

including sham group (sham operation)

CCI group [intrathecal injection of 10% dimethyl sulfoxide (DMSO)

]

and CCI+DHC group (intrathecal injection of DHC)

8 mice in each group. A CCI mouse model was conducted to induce neuropathic pain through ligating the right common sciatic nerve. On day 14 after CCI modeling or sham operation

mice were intrathecal injected with 5 μL of 10% DMSO or 10 mg/kg DHC (5 μL) into the 5th to 6th lumbar intervertebral space (L5–L6). Pregnant ICR mice were sacrificed for isolating primary spinal neurons on day 14 of embryo development for

in vitro

experiment. Pain behaviors were evaluated by measuring the paw withdrawal mechanical threshold (PWMT) of mice. Immunofluorescence was used to observe the activation of astrocytes and microglia in mouse spinal cord. Protein expressions of inducible nitric oxide synthase (iNOS)

tumor necrosis factor alpha (TNF-α)

interleukin 6 (IL-6)

phosphorylation of N-methyl-D-aspartate receptor subunit 2B (p-NR2B)

and NR2B in the spinal cord or primary spinal neurons were detected by Western blot.

Results:

2

In CCI-induced neuropathic pain model

mice presented significantly decreased PWMT

activation of glial cells

overexpressions of iNOS

TNF-α

IL-6

and higher p-NR2B/NR2B ratio in the spinal cord (

P

<

0.05 or

P

<

0.01)

which were all reversed by a single intrathecal injection of DHC (

P

<

0.05 or

P

<

0.01). The p-NR2B/NR2B ratio in primary spinal neurons were also inhibited after DHC treatment (

P

<

0.05).

Conclusion:

2

An intrathecal injection of DHC relieved CCI-induced neuropathic pain in mice by inhibiting the neuroinflammation and neuron hyperactivity.