通过氧化应激介导的脊柱内omorphin-2的下降有助于大鼠的腰椎椎间盘椎间盘 sciatica
Le Niu1, Chun-Jiang Zuo2, Yong-Ling Zhang2
1Haojing College of Shaanxi University of Science＆Technology, Unified Avenue, Xianyang, 712046, PR China; The Xi'an DaXing Hospital, 353 Laodong North Road, Xi'an, 710016, PR China.
Neurochemistry international
|May 10, 2024
概括
氧化应激会降低脊髓和背部根腺中的内蒙基因-2 (EM2) 水平,导致腰椎椎间盘 (LDHS) 的疼痛. 抗氧化剂治疗通过恢复EM2水平来缓解LDHS疼痛.
科学领域:
- 神经科学是一个神经科学.
- 疼痛研究 疼痛研究
- 生物化学 生物化学
背景情况:
- 腰椎间盘椎间盘 sciatica (LDHS) 涉及氧化应激,但其神经机制仍然不清楚.
- 类阿片受体 (MOR) 的内源连接体Endomorphin-2 (EM2) 与神经病痛有关.
- 了解EM2在LDHS中的作用对于开发有针对性的疼痛疗法至关重要.
研究的目的:
- 调查内蒙基因-2 (EM2) 和氧化应激在腰椎椎间板椎间板 sciatica (LDHS) 的神经机制中的作用.
- 探索氧化应激对EM2表达的影响及其对LDHS相关疼痛的贡献.
- 评估针对EM2通路和LDHS中氧化应激的治疗潜力.
主要方法:
- 建立了一个核脉植入诱导的LDHS大鼠模型.
- 评估了背部根结节 (DRG) 和脊髓中的机械体,EM2表达和氧化应激标志物.
- 研究了二二酶IV活性在EM2降低中的作用.
- 使用全身抗氧化剂和内MOR抗剂/EM2来评估疼痛调节.
主要成果:
- LDHS大鼠在DRG和脊髓中表现出降低EM2表达和增加氧化应激.
- 氧化应激诱导的双二酶IV活性增加是EM2减少的原因.
- 抗氧化剂治疗防止了机械体,而MOR抗剂加剧了疼痛.
- 内EM2表现出强大的止痛作用,超过了内蒙啡-1和吗啡.
结论:
- 氧化应激介导的脊柱EM2的减少,通过减少内源性止痛作用,有助于LDHS的病理生理学.
- 向氧化应激和增强EM2/MOR通路是LDHS疼痛管理的有希望的治疗策略.
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