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化疗治疗疼痛:用抗癌药物密拉美A逆转炎症和神经病痛

Zheyun Xu¹, Man-Cheung Lee¹, Kayla Sheehan¹

¹Department of Anesthesia and Perioperative Care and the UCSF Pain and Addiction Research Center, University of California, San Francisco, San Francisco, CA, United States.

|June 27, 2023

概括

甲基氨酸 (MTM) 通过向基因网络来逆转炎症和化疗诱导的外围神经病变 (CIPN) 疼痛. 这表明持续性疼痛是由可修改的,依赖转录的过程维持的,提供了一种新的治疗方法.

科学领域:

神经科学是一个神经科学.
药理学药理学是指药理学的学科.
分子生物学分子生物学

背景情况:

持续性炎症和神经病痛的机制尚不清楚.
类似Sp1的转录因子调节疼痛受体TRPV1,并被mithramycin A (MTM) 抑制.

研究的目的:

调查MTM在逆转炎症和化疗诱导的外围神经病变 (CIPN) 疼痛的体内模型中的有效性.
探索MTM扭转疼痛效应的分子机制.

主要方法:

在Friend辅助剂诱导的炎症性疼痛和oxaliplatin诱导的CIPN模型中对MTM的体内评估.
转录形状 (RNAseq) 和基因表达,替代拼接和线粒体功能的分析在背部根质神经元 (DRG) 中.

主要成果:

在CIPN模型中,MTM逆转了炎症性疼痛和热,机械和寒冷过敏的热过敏症.
在没有恢复神经纤维的情况下,MTM逆转了氧沙胺诱导的TRPM8过度表达和冷过敏.
在DRG神经元中,MTM逆转了线粒体电子运输链基因因因氧化诱导的失调,并减少了DRG神经元中的活性氧物种.

结论:

通过广泛的转录和替代拼接调节,MTM可以逆转炎症和神经病痛.
像CIPN这样的持续性疼痛状态是由持续的,可修改的转录依赖过程维持的.
通过准这些潜在的转录机制,MTM显示出作为治疗持续性疼痛的治疗剂的潜力.

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