The function of
microRNAs (
miRNAs or miRs) in regulating
neuropathic pain has attracted increasing attention in recent years. However, the precise mechanism of
miRNAs in
neuropathic pain remains largely unknown. In the present study, an important role of miR‑141 and its putative target gene, high‑mobility group box‑1 (
HMGB1), was demonstrated in a rat model of
neuropathic pain induced by chronic constriction injury (CCI). The expression of miR‑141 was significantly downregulated in the dorsal root ganglion of rats following CCI surgery. Overexpression of miR‑141 by
intrathecal injection of miR‑141 precursor mediated by a lentivirus‑derived gene transfer significantly inhibited
mechanical allodynia,
thermal hyperalgesia and proinflammatory
cytokine release in CCI rats. Using a dual
luciferase reporter assay, a direct interaction between miR‑141 and the 3'‑untranslated region of
HMGB1 was verified. Overexpression of miR‑141 significantly suppressed the expression of
HMGB1 in vitro and in vivo. Furthermore, overexpression of
HMGB1 apparently abrogated the beneficial effect of miR‑141 on inhibiting
neuropathic pain. Taken together, the data suggest that overexpression of miR‑141 alleviates
neuropathic pain development via targeting and inhibiting
HMGB1, implying that blocking
HMGB1 by miR‑141 could be a useful therapeutic strategy for the treatment of
neuropathic pain.