西诺因通过促进p65无化和调节微质极化来缓解癌症引起的骨疼痛
Xueqin Sun1, Dongbo Cao1, Wuping Li2
1Department of Pain Treatment, The First Hospital of Hunan University of Chinese Medicine, Changsha, Hunan, China.
The Journal of pharmacology and experimental therapeutics
|October 23, 2025
概括
西诺因 (SIN) 通过减少炎症和疼痛,有效治疗癌症引起的骨疼痛 (CIBP). 这项研究表明,SIN抑制NF-κB通路,为CIBP提供了一个有前途的治疗选择.
科学领域:
- 药理学和毒理学 药理学和毒理学
- 神经科学是一个神经科学.
- 在瘤学瘤学.
背景情况:
- 癌症引起的骨疼痛 (CIBP) 是骨转移的严重并发症,需要有效的治疗.
- 西诺胺 (SIN) 是来自Sinomenium acutum的类,已知具有抗炎和止痛的特性.
- 在管理CIBP时,SIN的精确机制在很大程度上仍未被探索.
研究的目的:
- 调查Sinomenine (SIN) 在缓解癌症引起的骨疼痛 (CIBP) 的疗效.
- 在大鼠CIBP模型中阐明SIN作用的潜在分子机制.
- 评估SIN对微质激活和炎症通路的影响.
主要方法:
- 通过瘤植入,建立了CIBP的雌性大鼠模型.
- 行为评估 (机械体,自发活动) 用于评估疼痛.
- 免疫光测试和分子分析 (NF-κB信号传递,泛化测试) 在CIBP大鼠和LPS治疗的BV2微质细胞上进行.
主要成果:
- 在CIBP大鼠中,SIN的使用显著降低了机械旋和门诊缺陷.
- SIN抑制了促炎性微质偏向 (M1表型) 并促进了抗炎性表型 (M2).
- 通过诱导p65泛化和蛋白质体降解,SIN减弱了NF-κB信号,p65过度表达逆转了SIN的影响.
结论:
- 在癌症引起的骨疼痛 (CIBP) 的临床前模型中,Sinomenine (SIN) 显示出显著的止痛和抗炎作用.
- SIN通过抑制NF-κB信号通路来发挥其治疗作用,通过依赖于ubiquitination的p65.5降解抑制NF-κB信号通路.
- 这些发现突出了SIN作为管理CIBP的潜在治疗剂,提供疼痛缓解和抗炎作用.
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