中国神经再生研究(英文版)

中国神经再生研究(英文版) ›› 2022, Vol. 17 ›› Issue (12): 2778-2784.doi: 10.4103/1673-5374.339494

• 原著:周围神经损伤修复保护与再生 • 上一篇    

11-羟基-β-乙酰乳香酸促进坐骨神经损伤修复的分子机制

  

  • 出版日期:2022-12-15 发布日期:2022-05-05
  • 基金资助:
    国家自然科学基金项目（31972725）

Acetyl-11-keto-beta-boswellic acid promotes sciatic nerve repair after injury: molecular mechanism

Yao Wang1, Zong-Liang Xiong1, Xiang-Lin Ma1, Chong Zhou1, Mo-Han Huo2, Xiao-Wen Jiang1, *, Wen-Hui Yu1, 3, 4, *   

  1. 1Department of Veterinary Medicine, Northeast Agricultural University, Harbin, Heilongjiang Province, China; 2College of Life Sciences, Northeast Agricultural University, Harbin, Heilongjiang Province, China; 3Key Laboratory of Heilongjiang Education Department for Common Animal Disease Prevention and Treatment, Northeast Agricultural University, Harbin, Heilongjiang Province, China; 4Institute of Chinese Veterinary Medicine, Northeast Agricultural University, Harbin, Heilongjiang Province, China
  • Online:2022-12-15 Published:2022-05-05
  • Contact: Xiao-Wen Jiang, PhD, jiangxiaowen@neau.edu.cn; Wen-Hui Yu, PhD, yuwenhui@neau.edu.cn.
  • Supported by:
    This study was supported by the National Natural Science Foundation of China, No. 31972725 (to WHY).

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摘要：

既往研究已发现天然药物乳香中的活性成分11-羟基-β-乙酰乳香酸，可通过促进许旺细胞增殖，促进坐骨神经损伤的修复，但其分子水平的机制尚不明确。实验首先对11-羟基-β-乙酰乳香酸灌胃30d的坐骨神经挤压伤大鼠模型进行基因组学分析，发现与11-羟基-β-乙酰乳香酸治疗相关的通路为吞噬体通路，且神经营养因子信号通路中脑源性神经营养因子也出现显著上调。因此进一步探索吞噬体通路和神经营养因子信号通路中基因和蛋白的变化，发现吞噬体通路中髓过氧化物酶的表达明显降低，而神经营养因子信号通路中脑源性神经营养因子、神经生长因子和神经生长因子受体表达显著上升，同时炎症因子CD68、白细胞介素1β、白细胞介素1β前体以及肿瘤坏死因子α水平下降，且损伤坐骨神经髓鞘碱性蛋白和β3微管蛋白阳性表达以及G比例增加。提示在分子水平上，11-羟基-β-乙酰乳香酸可通过抑制髓过氧化物酶表达以及炎症反应，促进神经营养因子表达，进而促进损伤坐骨神经髓鞘和轴突的再生。

https://orcid.org/0000-0002-4515-6266 (Xiao-Wen Jiang); https://orcid.org/0000-0002-3744-4575 (Wen-Hui Yu)

关键词: 周围神经, 基因组学, 吞噬体通路, 炎症反应, 神经营养因子, 神经损伤, 神经修复, 乳香, 髓鞘, 神经纤维

Abstract: Previous studies showed that acetyl-11-keto-beta-boswellic acid (AKBA), the active ingredient in the natural Chinese medicine Boswellia, can stimulate sciatic nerve injury repair via promoting Schwann cell proliferation. However, the underlying molecular mechanism remains poorly understood. In this study, we performed genomic sequencing in a rat model of sciatic nerve crush injury after gastric AKBA administration for 30 days. We found that the phagosome pathway was related to AKBA treatment, and brain-derived neurotrophic factor expression in the neurotrophic factor signaling pathway was also highly up-regulated. We further investigated gene and protein expression changes in the phagosome pathway and neurotrophic factor signaling pathway. Myeloperoxidase expression in the phagosome pathway was markedly decreased, and brain-derived neurotrophic factor, nerve growth factor, and nerve growth factor receptor expression levels in the neurotrophic factor signaling pathway were greatly increased. Additionally, expression levels of the inflammatory factors CD68, interleukin-1β, pro-interleukin-1β, and tumor necrosis factor-α were also decreased. Myelin basic protein- and β3-tubulin-positive expression as well as the axon diameter-to-total nerve diameter ratio in the injured sciatic nerve were also increased. These findings suggest that, at the molecular level, AKBA can increase neurotrophic factor expression through inhibiting myeloperoxidase expression and reducing inflammatory reactions, which could promote myelin sheath and axon regeneration in the injured sciatic nerve.

Key words: AKBA, axon, genomics, inflammatory, injury and repair, myelin sheath, myeloperoxidase, neurotrophic factor, peripheral nerve, phagosome pathway, regeneration, Sprague-Dawley rat