Wang Yao, Xiong Zong-Liang, Ma Xiang-Lin, Zhou Chong, Huo Mo-Han, Jiang Xiao-Wen, Yu Wen-Hui
Department of Veterinary Medicine, Northeast Agricultural University, Harbin, Heilongjiang Province, China.
College of Life Sciences, Northeast Agricultural University, Harbin, Heilongjiang Province, China.
Neural Regen Res. 2022 Dec;17(12):2778-2784. doi: 10.4103/1673-5374.339494.
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.
先前的研究表明，天然中药乳香中的活性成分乙酰-11-酮-β-乳香酸（AKBA）可通过促进雪旺细胞增殖来刺激坐骨神经损伤修复。然而，其潜在的分子机制仍知之甚少。在本研究中，我们对胃内给予AKBA 30天的大鼠坐骨神经挤压损伤模型进行了基因组测序。我们发现吞噬体途径与AKBA治疗有关，并且神经营养因子信号通路中的脑源性神经营养因子表达也高度上调。我们进一步研究了吞噬体途径和神经营养因子信号通路中的基因和蛋白质表达变化。吞噬体途径中的髓过氧化物酶表达明显降低，神经营养因子信号通路中的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水平大幅增加。此外，炎症因子CD68、白细胞介素-1β、前白细胞介素-1β和肿瘤坏死因子-α的表达水平也降低。损伤坐骨神经中的髓鞘碱性蛋白和β3-微管蛋白阳性表达以及轴突直径与总神经直径之比也增加。这些发现表明，在分子水平上，AKBA可通过抑制髓过氧化物酶表达和减少炎症反应来增加神经营养因子表达，这可能促进损伤坐骨神经中的髓鞘和轴突再生。
