Expression of high mobility group box 1 protein in deafferentation pain rat models and its relation with neuroinflammation
10.3760/cma.j.cn115354-20200120-00048
- VernacularTitle:HMGB1在去传入神经病理性疼痛模型大鼠中的表达及其与神经炎症的关系研究
- Author:
Ao CHEN
1
;
Zhenzhong ZHONG
;
Xiaoming LI
;
Zhiqiang FA
Author Information
1. 国家临床重点专科，教育部工程技术研究中心，广东省脑功能修复与再生重点实验室，南方医科大学珠江医院神经外科，广州 510282
- Keywords:
Deafferentation pain;
High mobility group box 1 protein;
Microglia;
Behavioral change
- From:
Chinese Journal of Neuromedicine
2020;19(5):454-461
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate the expression characteristics of high mobility group box 1 protein (HMGB1) in rat models of deafferentation pain induced by posterior root injury of spinal nerves, and its relation with neuroinflammation.Methods:Sixty SD rats were divided into a blank control group ( n=10) and a model group ( n=50) according to random number table method. Neuropathic pain rat models in the model group were established by cutting the posterior root of C 5-T 1 spinal nerve, while rats in the control group were performed the same operation without cutting the posterior root of C 5-T 1 spinal nerve. Three, 7, 10, 14, and 21 d after modeling, behavioral changes, including spontaneous pain scale scores, mechanical antagonistic pain threshold, and autophagy scale scores, were evaluated in the two groups of rats. Immunohistochemical staining was used to detect the HMGB1, ionized calcium binding adapter molecule 1 (IBA-1) and phosphorylated nuclear factor κB (pNF-κB) positive cells in the spinal cord of the two groups. Western blotting was used to detect the protein expressions of HMGB1, toll-like receptor (TLR)2 and pNF-κB in the spinal cord of the two groups. Results:(1) The scores of spontaneous pain scale and autophagy scale 14 and 21 d after modeling were significantly higher than those 3, 7 and 10 d after modeling ( P<0.05), and those 21 d after modeling were significantly higher than those 14 d after modeling ( P<0.05). (2) Immunohistochemical staining showed that HMGB1, IBA-1 and pNF-κB all expressed in the spinal cord tissues of rats in the model group 3 d after modeling, and the number of positive cells in the dorsal horn of the spinal cord on the injured side became larger with prolongation of exposure time, and that was obviously larger as compared with that on the opposite side; in the spinal cord tissues of the blank control group, the number of positive cells in the spinal dorsal horn area was small, and there was no significant difference in the number of positive cells in the spinal dorsal horn area on both sides. (3) Western blotting showed that, as compared with those in the blank control group, HMGB1, TLR2 and pNF-κB protein expressions in the spinal cord tissues of the model group were significantly increased 3, 7, 10, 14 and 21 d after modeling ( P<0.05), and which showed an increasing trend with prolongation of exposure time. Conclusion:The gradual increase in HMGB1 expression in the local spinal cord of rats with deafferentation pain leads to HMGB1/TLR2/NF-κB pathway high expression and activation of microglia cells, which induces the occurrence of local neuroinflammation in the spinal cord and eventually results in pain behavioral changes.
