Abstract
Objective Neuropathic pain with complex mechanisms has become a major public health problem that greatly impacts patients' quality of life. Therefore, novel and more effective strategies against neuropathic pain need further investigation. Electroacupuncture (EA) has an ameliorating effect on neuropathic pain following spared nerve injury (SNI), but the underlying mechanism remains to be fully clarified. Interferon regulatory factor 8 (IRF8), a critical transcription factor, was reported to be involved in the modulation of neuropathic pain. Here, we focused on exploring whether 2 Hz EA stimulation exerts an inhibitory action on spinal IRF8 in SNI rats. Methods In this study, SNI rats were treated with 2 Hz EA once every other day for 21 days. Paw withdrawal threshold (PWT) was applied to determine the analgesic effect of 2 Hz EA on SNI rats. The spinal IRF8 and CX3CRl expressions were detected with qRT-PCR and western blot, and immunofluorescence staining was used to evaluate colocation of IRF8 or CX3CRl with microglial activation marker CD11b in the spinal cord. Results It was found that SNI induced significant elevation of spinal IRF8 and CX3CRl mRNA and protein expression. Additionally, immunofluorescence results showed that SNI elicited the coexpression of IRF8 with CD11b, as well as CX3CRl with CD11b in the spinal cord. Meanwhile, 2 Hz EA treatment of SNI rats not only reduced IRF8 and CX3CRl mRNA and protein expression, but also reversed the coexpression of IRF8 or CX3CRl with CD11b in the spinal cord, along with an attenuation of SNI-evoked mechanical hypersensitivity. Conclusion This experiment highlighted that 2 Hz EA can inhibit IRF8 expression and microglial activation in the spinal cord of SNI rats. Hence, targeting IRF8 may be a promising therapeutic strategy for 2 Hz EA treatment of neuropathic pain.
Highlights
Neuropathic pain resulting from peripheral nerve injury severely affects millions of individuals and causes a great burden to the health care [1]
To investigate the effect of 2 Hz EA treatment on mechanical hypersensitivity induced by spared nerve injury (SNI), SNI rats were treated with 2 Hz EA once every other day lasting for 21 days postsurgery, and the Paw withdrawal threshold (PWT) was measured
E results are shown in Figure 2; in comparison with the sham group, the PWT was significantly decreased in the SNI group (P < 0.001), which suggested that the rat model of SNI-induced neuropathic pain was successfully established
Summary
Neuropathic pain resulting from peripheral nerve injury severely affects millions of individuals and causes a great burden to the health care [1]. Neuropathic pain is closely associated with hyperalgesia, allodynia, and spontaneous pain. The mechanisms underlying neuropathic pain are well complicated [1]. It is evident that nerve injury induces the activation of microglia in the spinal cord [2, 3], and the activated microglia can evoke central sensitization and lead to neuropathic pain [4, 5]. Some transcription factors participate in the modulation of microglial activation [6]. Recent studies reported that interferon regulatory factor 8
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