Involvement of spinal SIRT1 in development of chronic constriction injury induced neuropathic pain in rats.

It is known that the epigenetic process of histone acetylation is involved in the neuropathic pain. The aim of this study was to determine whether sirtuin type 1 (SIRT1), an NAD ⁺ dependent deacetylase, affected allodynia and hyperalgesia in neuropathic pain. The neuropathic pain model was established by ligature of the right sciatic nerve to induce chronic constriction injury (CCI) in rats. Histone acetyltransferase (HAT) activity was increased and, and histone deacetylase (HDAC) activity was declined in tissue of the spinal dorsa horn in CCI rates by means of enzyme-linked immunosorbent assay (ELISA). The persistent hyperalgesia and allodynia caused by CCI were associated with downregulation of SIRT1 and upregulation of acetylated-H3 (Ac-H3) in tissue of the spinal cord by Western blot assay, which was reversed after intrathecal injection of SIRT1 agonist SRT1720. SRT1720 treatment achieved analgesic through inhibiting the acetylation of nuclear factor kappa B (NF-κB) and blocking the releases of the inflammatory factors including tumor necrosis factor-α (TNF-α) and interleukin (IL)-6 by means of Western blot and real-time quantitative PCR (RT-PCR), respectively. Taken together, these data suggest that SIRT1 in the spinal cord plays an important role in the neuropathic pain in the rat model.
Competing Interests: None.
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