Open AccessElectroacupuncture Suppresses Mechanical Allodynia and Nuclear Factor Kappa B Signaling in Streptozotocin‐Induced Diabetic Rats
Author(s) -
Shi Lei,
Zhang HongHong,
Xiao Ying,
Hu Ji,
Xu GuangYin
Publication year - 2013
Publication title -
cns neuroscience and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.403
H-Index - 69
eISSN - 1755-5949
pISSN - 1755-5930
DOI - 10.1111/cns.12035
Subject(s) - electroacupuncture , streptozotocin , medicine , intraperitoneal injection , allodynia , dorsal root ganglion , endocrinology , subcutaneous injection , pharmacology , hyperalgesia , diabetes mellitus , diabetic neuropathy , analgesic , neuropathic pain , spinal cord , nociception , acupuncture , receptor , pathology , alternative medicine , psychiatry
Summary Aims To investigate whether electroacupuncture ( EA ) produced analgesic effect and whether nuclear factor kappa B ( NF ‐κ B ) and cystathionine β synthase ( CBS ) involved in EA ‐mediated analgesia in painful diabetic neuropathy in rats. Methods Diabetes was induced by an intraperitoneal injection of streptozotocin ( STZ ) in adult female rats. Mechanical pain threshold was measured by von Frey filaments. EA was applied at acupoint Z u‐ S an‐ L i ( ST ‐36) in both hindlimbs. Western blot analysis was employed to detect changes in protein levels of NF ‐κB and CBS in spinal dorsal root ganglion ( DRG s). Results Mechanical allodynia was developed 2 weeks after STZ injection and lasted for another 4 weeks. STZ injection significantly enhanced expression of p65 and CBS in lumbar L 4‐6 DRG s when compared with age‐matched controls. EA markedly attenuated mechanical allodynia. Importantly, EA treatment remarkably inhibited p65 and CBS expression in DRG s. Additionally, intrathecal injection of the p65 antagonist pyrrolidine dithiocarbamate attenuated mechanical allodynia and markedly inhibited CBS expression in DRG s in STZ rats. Conclusions These data indicate that EA produced an analgesic effect, which might be mediated at least in a part by inhibition of NF ‐κB signaling pathway in primary sensory neurons in rats with diabetes.