Baicalin relieves neuropathic pain by regulating α(2)-adrenoceptor levels in rats following spinal nerve injury

In the present study, the ability of baicalin to relieve neuropathic pain due to spinal nerve ligation in rats was explored, and the relationship between baicalin and α(2)-adrenoceptors (α(2)-AR) was determined. The neuropathic pain model was established by ligating the L5-L6 spinal nerves in Sprague-Dawley rats. Several α(2)-AR antagonists were injected into the intramedullary sheath to evaluate the role of baicalin in neuropathic pain. The antagonists included nonselective α(2)-AR antagonist idazoxan, α(2a)-AR antagonist BRL 44408, α(2b)-AR antagonist ARC 239 and α(2c)-AR antagonist JP 1302. The rats were divided into an untreated control group, saline group, baicalin group and baicalin + α(2)-AR antagonist groups. Paw withdrawal threshold (PWT) was tested to assess the level of pain felt by the rats. The levels of α(2)-AR mRNA were tested by reverse transcription-quantitative PCR. Inflammatory factors, including tumor necrosis factor (TNF)-α, interleukin (IL)-6, IL-17 and IL-1β, were analyzed by ELISA. The histopathological changes were assessed by hematoxylin and eosin staining. Flow cytometry was used to examine the percentage of CD4(+) peripheral blood mononuclear cells (PBMCs). Compared with the saline group, the PWT value increased after treating with baicalin. However, intrathecal injection of α(2)-AR antagonist reversed the antinociceptive effects of baicalin. Compared with the saline group, the expression of α(2a)-AR and α(2c)-AR mRNA was upregulated significantly in the baicalin group (P<0.05). Levels of α(2)-AR mRNA were also decreased in the baicalin + idazoxan group compared with the baicalin group (P<0.05). The levels of TNF-α, IL-6, IL-17 and IL-1β were raised after treatment with baicalin. In addition, baicalin treatment ameliorated the histological damage in the spinal cord. The percentage of CD4(+) PBMCs was increased in the saline group compared with the control group (P<0.05). Compared with the baicalin group, the percentage of CD4+ PBMCs was raised after treatment with the α(2)-AR antagonists. In conclusion, intrathecal injection of baicalin produced an antiallodynic effect in a spinal nerve ligation-induced neuropathic pain model. The mechanism may be related to the regulation of a(2)-AR expression.