西诺因通过促进CRMP2的酸化和核转位来改善纤维细胞样同胞细胞功能障碍
Jie Yu1, Song Wang2, Si-Jia Chen2
1The Second Affiliated Hospital of Zhejiang Chinese Medical University, Xinhua Hospital of Zhejiang Province, Hangzhou, 310053, China; College of Basic Medical Science, Key Laboratory of Neuropharmacology and Translational Medicine of Zhejiang Province, Zhejiang Chinese Medical University, Hangzhou, 310058, China.
Journal of ethnopharmacology
|January 4, 2024
概括
西诺明因 (SIN) 通过减少关节炎症和疼痛来缓解类风湿性关节炎 (RA). 它通过调节纤维细胞样同胞细胞 (FLS) 中的CRMP2 T514酸化来实现这一目标,抑制炎症性细胞因子的释放,并抑制异常细胞入侵和迁移.
科学领域:
- 类风湿病学 类风湿病学
- 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:
- 类风湿性关节炎 (RA) 是一种慢性自身免疫性疾病,导致关节炎症和疼痛.
- 来自Sinomenium acutum的Sinomenine (SIN) 传统上用于RA,具有抗炎和止痛作用.
- SIN对关节病理和纤维细胞样同胞细胞 (FLS) 的确切机制尚不清楚.
研究的目的:
- 为了研究SIN对关节炎的治疗作用,在一个由原诱导的关节炎 (CIA) 的大鼠模型中.
- 阐明SIN对FLS功能障碍的作用的潜在分子机制,包括炎症,入侵和迁移.
主要方法:
- 通过组织病理学评估SIN的治疗效果在老鼠CIA模型中进行了评估.
- 在体外研究中使用LPS诱导的FLS来评估SIN对炎症因素,入侵和迁移的影响.
- 分析了CRMP2蛋白表达,T514的酸化及其核转位,并使用qPCR,ELISA,Western Blot和免疫光.
主要成果:
- 在CIA大鼠中,SIN治疗改善了关节病理,减少了膜炎症和软骨损伤.
- SIN抑制了LPS诱导的促炎细胞因子的释放,并以剂量依赖的方式抑制了FLS的入侵和迁移.
- SIN降低了LPS诱导的CRMP2表达,但增加了它的T514酸化,促进了核转移并影响了FLS的功能.
结论:
- 在RA中,SIN通过调节CRMP2 T514酸化和FLS中的核转移来发挥抗炎和止痛作用.
- 抑制促炎性细胞因子释放和抑制异常FLS的入侵/迁移是关键机制.
- CRMP2 T514酸化代表了RA相关关节破坏和疼痛的潜在治疗标.
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