Chronic
neuropathic pain is an unfavourable pathological
pain characterised by
allodynia and
hyperalgesia which has brought considerable trouble to people's physical and mental health, but effective
therapeutics are still lacking.
MicroRNAs (
miRNAs) have been widely studied in the development of
neuropathic pain and neuronal
inflammation. Among various
miRNAs, miR-155 has been widely studied. It is intensively involved in regulating
inflammation-associated diseases. However, the role of miR-155 in regulating
neuropathic pain development is poorly understood. In the present study, we aimed to investigate whether miR-155 is associated with
neuropathic pain and delineate the underlying mechanism. Using a
neuropathic pain model of chronic constriction injury (CCI), miR-155 expression levels were markedly increased in the spinal cord. Inhibition of miR-155 significantly attenuated
mechanical allodynia,
thermal hyperalgesia and proinflammatory
cytokine expression. We also demonstrated that miR-155 directly bound with the 3'-untranslated region of the suppressor of
cytokine signalling 1 (SOCS1). The expression of SOCS1 significantly decreased in the CCI rat model, but this effect could be reversed by miR-155 inhibition. Furthermore, knockdown of SOCS1 abrogated the inhibitory effects of miR-155 inhibition on neuropathic development and neuronal
inflammation. Finally, we demonstrated that inhibition of miR-155 resulted in the suppression of nuclear factor-κB and
p38 mitogen-activated protein kinase activation by mediating SOCS1. Our data demonstrate the critical role of miR-155 in regulating
neuropathic pain through SOCS1, and suggest that miR-155 may be an important and potential target in preventing
neuropathic pain development.