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Resveratrol Facilitates Pain Attenuation in a Rat Model of Neuropathic Pain Through the Activation of Spinal Sirt1
  1. Qin Yin, MD*,,,
  2. Fei-Fei Lu, MD*,,
  3. Yu Zhao*,,
  4. Ming-Yue Cheng, MD*,,,
  5. Qin Fan, MD*,,
  6. Jie Cui, MD*,,
  7. Lei Liu, MD*,,
  8. Wei Cheng, MD*,, and
  9. Chang-Dong Yan, MD*,
  1. From *Xuzhou Medical College, †Jiangsu Province Key Laboratory of Anesthesiology and Center for Pain Research and Treatment, and ‡Affiliated Hospital of Xuzhou Medical College, Xuzhou, China.
  1. Address correspondence to: Chang-Dong Yan, MD, Xuzhou Medical College, Xuzhou 221002, China (e-mail: yancd55{at}; Wei Cheng, MD, Xuzhou Medical College, Xuzhou 221002, China (e-mail: cheng.wei.1{at}


Background Little research has been conducted regarding the implications of Sirt1 (a classic III HDAC) in neuropathic pain. The aim of this study was to investigate the variation in the expressions of spinal Sirt1 and acetyl-histone H3 in a rat model of chronic constriction injury.

Methods A neuropathic pain model of chronic constriction injury (CCI) was established in a unilateral hind limb in Sprague-Dawley rats.

Results Western blot analysis and immunohistochemistry revealed that Sirt1 (silent information regulator) expression decreased, whereas acetyl-histone H3 increased in the spinal cord following CCI surgery. The intrathecal administration of resveratrol, an activator of Sirt1, attenuated CCI-induced mechanical allodynia and thermal hyperalgesia, increased Sirt1 expression, and decreased acetyl-histone H3 in the spine. Resveratrol induced no obvious histopathological changes in the spinal cord.

Conclusions Our data provide new evidence for the contribution of spinal Sirt1 to the initiation and maintenance of neuropathic pain. The antinociceptive effects of resveratrol may be mediated through the activation of spinal Sirt1 in CCI rats.

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  • Joseph M. Neal, MD, served as editor-in-chief for this article.

    Q.Y. and F.-F.L. contributed equally to this study.

    This work was supported by the National Natural Science Foundation of China (31100801, 81200858).

    The authors declare no conflict of interest.