Effects of palmatine on BDNF/TrkB-mediated trigeminal neuralgia

Effects of palmatine on BDNF/TrkB-mediated trigeminal neuralgia
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巴马汀对 BDNF/TrkB 介导的三叉神经痛的影响。

DOI:
10.1038/s41598-020-61969-1
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发表时间:
2020-03-19
期刊:
影响因子:
4.6
通讯作者:
Xiong, Wei
Xiong, Wei
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Liu, Lijuan;He, Lingkun;Xiong, Wei

文献摘要

被引文献

相似文献

三叉神经痛(TN)是三叉神经分布区的一种突发性、针刺样疼痛,严重影响患者的身心健康。在包括TN在内的慢性疼痛条件下,脑源性神经营养因子(BDNF)水平的增加可能会增强疼痛传递。本研究比较了巴马汀给药对假手术组和TN模型组Sprague-Dawley大鼠三叉神经节细胞BDNF及其受体Trk B(原肌球蛋白受体激酶B)表达的影响。术后14天内,TN组的机械痛敏阈值明显低于假手术组,而TN +巴马汀组的机械痛敏阈值高于TN组(p < 0.05)。实时定量PCR、免疫组化和免疫荧光检测显示,TN组BDNF和TrkB的表达高于Sham组,而巴马汀治疗可逆转这些变化。Western blotting结果显示巴马汀可降低TN大鼠细胞外信号调节激酶1/2(ERK 1/2)的磷酸化水平。因此,BDNF/TrkB通路可能参与TN的疼痛传递过程,巴马汀治疗可能通过抑制BDNF/TrkB通路和抑制ERK 1/2磷酸化来减少疼痛传递。
Trigeminal neuralgia (TN), a sudden, needle-like pain in the distribution area of the trigeminal nerve, can seriously affect the physical and mental health of patients. In chronic pain conditions including TN, increased levels of brain-derived neurotrophic factor (BDNF) may enhance pain transmission. This study compares the effect of palmatine administration on the expression of BDNF and its receptor TrkB (tropomyosin receptor kinase B) in trigeminal ganglion cells of Sprague-Dawley rats in a sham versus TN model group. Within 14 days of surgery, the mechanical allodynia threshold of the TN group was significantly lower than that of the sham group, while the TN + palmatine group had a higher mechanical pain sensitivity threshold than the TN group (p < 0.05). Real-time quantitative PCR, immunohistochemistry, and immunofluorescence showed that BDNF and TrkB expression in the TN group was higher than that in the sham group, while palmatine treatment could reverse these changes. Western blotting showed that palmatine treatment could reduce the elevated phosphorylation of extracellular signal-regulated kinases 1/2 (ERK1/2) in TN rats. Thus, the BDNF/TrkB pathway may be involved in the pain transmission process of TN, and palmatine treatment may reduce pain transmission by inhibiting the BDNF/TrkB pathway and suppressing ERK1/2 phosphorylation.