利多卡因激活星形胶质细胞的自噬并改善慢性收缩损伤引起的神经性疼痛,The Journal of Biochemistry

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利多卡因激活星形胶质细胞的自噬并改善慢性收缩损伤引起的神经性疼痛
The Journal of Biochemistry ( IF 2.1 ) Pub Date : 2020-11-27 , DOI: 10.1093/jb/mvaa136
Jiaqi Yuan ₁ , Yue Fei ₁

Affiliation

摘要

利多卡因是缓解神经性疼痛 (NP) 的常用药物。本工作旨在探讨利多卡因减轻 NP 的机制。慢性缩窄性损伤 (CCI) 大鼠通过手术诱导 NP 建立。我们观察了大鼠的机械戒断阈值（MWT）和热戒断潜伏期（TWL）。进行免疫荧光染色以确定 LC3/胶质纤维酸性蛋白 (GFAP) 阳性细胞。用脂多糖（LPS）处理大鼠星形胶质细胞以诱导CCI，然后用利多卡因或3-MA（自噬抑制剂）处理。进行CCK-8以检测细胞增殖。进行蛋白质印迹和酶联免疫吸附试验以检测蛋白质和炎症因子的水平。CCI 大鼠表现出 MWT 和 TWL 的降低，利多卡因有效地消除了这种降低。利多卡因增加了 CCI 大鼠中 LC3/GFAP 阳性细胞的数量。此外，利多卡因抑制 GFAP 和 p62 的表达，并增强 LPS 处理的星形胶质细胞中 LC3-II/LC3-I 的表达。利多卡因抑制 LPS 处理的星形胶质细胞中 TNF-α 和 IL-1β 的水平。3-MA 有效消除了利多卡因带来的影响。总之，我们的工作表明利多卡因激活星形胶质细胞的自噬并改善 CCI 诱导的 NP。因此，我们的研究为利多卡因减轻NP的机制提供了进一步的实验基础。3-MA 有效消除了利多卡因带来的影响。总之，我们的工作表明利多卡因激活星形胶质细胞的自噬并改善 CCI 诱导的 NP。因此，我们的研究为利多卡因减轻NP的机制提供了进一步的实验基础。3-MA 有效消除了利多卡因带来的影响。总之，我们的工作表明利多卡因激活星形胶质细胞的自噬并改善 CCI 诱导的 NP。因此，我们的研究为利多卡因减轻NP的机制提供了进一步的实验基础。

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Lidocaine activates autophagy of astrocytes and ameliorates chronic constriction injury-induced neuropathic pain

Abstract

Lidocaine is a commonly used drug to alleviate neuropathic pain (NP). This work aims to investigate the mechanism of lidocaine in alleviating NP. Chronic constriction injury (CCI) rats were established by surgery to induce NP. We observed the mechanical withdrawal threshold (MWT) and thermal withdrawal latency (TWL) of rats. Immunofluorescence staining was performed to determine the LC3/glial fibrillary acidic protein (GFAP)-positive cells. Rat astrocytes were treated with lipopolysaccharide (LPS) to induce CCI, and then treated with lidocaine or 3-MA (autophagy inhibitor). CCK-8 was performed to detect cell proliferation. Western blot and enzyme-linked immunosorbent assay were performed to detect the level of protein and inflammatory factor. CCI rats exhibited a decrease of MWT and TWL, which was effectively abolished by lidocaine. Lidocaine enhanced the number of LC3/GFAP-positive cells in CCI rats. Moreover, lidocaine inhibited the expression of GFAP and p62, and enhanced LC3-II/LC3-I expression in the LPS-treated astrocytes. Lidocaine inhibited the level of TNF-α and IL-1β in the LPS-treated astrocytes. The influence conferred by lidocaine was effectively abolished by 3-MA. In conclusion, our work demonstrates that lidocaine activates autophagy of astrocytes and ameliorates CCI-induced NP. Thus, our study provides a further experimental basis for the mechanism of lidocaine to alleviate NP.

更新日期：2020-11-27

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