Postherpetic neuralgia (PHN) is a form of neuropathic pain that has significant detrimental effects. This study seeks to explore the potential association between miR‐138‐5p and PHN. A PHN model was established by infecting rats with the varicella‐zoster virus. Following this, the expression level of miR‐138‐5p in spinal cord was quantified using RT‐qPCR. To further investigate its role, miR‐138‐5p levels were modulated through the intrathecal administration of a lentivirus. The abnormal pain sensitivity in the rats was assessed utilizing the paw withdrawal threshold (PWT). Additionally, the levels of glial fibrillary acidic protein (GFAP) and pro‐inflammatory cytokines (IL‐1β and TNF‐α) in spinal cord were measured by RT‐qPCR or enzyme‐linked immunosorbent assay (ELISA). Dual‐luciferase reporter assay was used to verify the binding relationship between miR‐138‐5p and ROCK2. miR‐138‐5p is downregulated in the spinal cord tissue of PHN rats. Notably, the overexpression of miR‐138‐5p significantly enhances the PWT in PHN rats. Furthermore, the elevation of miR‐138‐5p markedly mitigates the abnormal increase of GFAP and pro‐inflammatory factors. Mechanistically, ROCK2 has been identified as a downstream target of miR‐138‐5p. During the onset of PHN, ROCK2 is persistently upregulated, whereas the overexpression of miR‐138‐5p effectively inhibits this increase. Interestingly, the concurrent overexpression of miR‐138‐5p and ROCK2 can counteract the enhancement in PWT engendered solely by the upregulation of miR‐138‐5p, alongside the reduction in levels of GFAP, IL‐1β, and IL‐6. miR‐138‐5p plays a crucial role in modulating the development of PHN. In the context of PHN, miR‐138‐5p inhibits spinal cord inflammation and hyperalgesia by suppressing ROCK2.

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