Baicalin relieves neuropathic pain by regulating α2-adrenoceptor levels in rats following spinal nerve injury

Lan-Ji Huang; Shu-Shan Jia; Xue-Hua Sun; Xin-You Li; Fei-Fei Wang; Wei Li; Qing-Song Jin

doi:10.3892/etm.2020.9019

Baicalin relieves neuropathic pain by regulating α₂-adrenoceptor levels in rats following spinal nerve injury

Exp Ther Med. 2020 Sep;20(3):2684-2690. doi: 10.3892/etm.2020.9019. Epub 2020 Jul 17.

Authors

Lan-Ji Huang¹, Shu-Shan Jia¹, Xue-Hua Sun¹, Xin-You Li¹, Fei-Fei Wang¹, Wei Li¹, Qing-Song Jin²

Affiliations

¹ Department of Anesthesiology, Yantai Affiliated Hospital of Binzhou Medical University, Yantai, Shandong 264100, P.R. China.
² Department of Endocrinology, Yantai Affiliated Hospital of Binzhou Medical University, Yantai, Shandong 264100, P.R. China.

Abstract

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 α₂-adrenoceptors (α₂-AR) was determined. The neuropathic pain model was established by ligating the L5-L6 spinal nerves in Sprague-Dawley rats. Several α₂-AR antagonists were injected into the intramedullary sheath to evaluate the role of baicalin in neuropathic pain. The antagonists included nonselective α₂-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 + α₂-AR antagonist groups. Paw withdrawal threshold (PWT) was tested to assess the level of pain felt by the rats. The levels of α₂-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 α₂-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 α₂-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 α₂-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 a₂-AR expression.

Keywords: baicalin; neuropathic pain; spinal nerve ligation; α2-adrenoceptors.