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草药化合物塞法兰丁通过阻断巨细胞M1极化来减轻炎症性关节炎

Chenyang Lu¹, Rui-Juan Cheng², Qiuping Zhang²

¹Department of Rheumatology and Immunology, West China Hospital, Sichuan University, Chengdu 610041, China; Division of Rheumatology, Department of Internal Medicine, the Third Affiliated Hospital, Sun Yat-Sen University, Guangzhou 510630, China.

International immunopharmacology

|November 17, 2023

概括

塞法兰丁 (CEP) 通过抑制单细胞运动和促炎性巨细胞分化,减少了类风湿性关节炎 (RA) 模型中的关节炎和破坏. 这种药物显示出作为一种新型治疗RA的潜力.

科学领域:

免疫学免疫学免疫学
药理学药理学是指药理学的学科.
类风湿病学类风湿病学

背景情况:

风湿性关节炎 (RA) 是一种慢性炎症性疾病,其特点是关节的破坏.
塞法兰丁 (CEP) 对 RA 的治疗潜力及其潜在机制在很大程度上仍未被探索.
了解CEP对参与RA病变的免疫细胞的影响,对于开发新疗法至关重要.

研究的目的:

调查塞法兰丁 (CEP) 对原诱导性关节炎 (CIA) 的治疗作用,一种类风湿性关节炎 (RA) 的模型.
阐明CEP改善关节炎症和破坏的分子机制.
评估CEP在RA背景下对巨细胞两极分化和功能的影响.

主要方法:

将CEP给一个由原诱导的关节炎 (CIA) 的小鼠模型.
关节损伤的放射和组织学评估,以及血清细胞因子分析.
试验室研究涉及M1巨诱导,RNA测序,西部抹杀和代谢试验,以探索CEP对单细胞化学反应,极化和糖解的影响.

主要成果:

在CIA小鼠中,CEP治疗显著降低了突关节炎症和关节破坏.
CEP降低了像TNF-α这样的促炎细胞因子的调节,并减少了M1巨细胞的数量.
在体外,CEP通过降低CR2和ERK1/2信号的调节来抑制单细胞化学反应,通过阻断TLRs-MyD88/IRAK4-IRF5通路来抑制M1巨细胞极化,并抑制糖解.

结论:

塞法兰丁 (CEP) 有效地减轻了在实验性关节炎中的关节炎症和破坏.
CEP通过抑制单细胞化学反应和促炎M1巨细胞分化来发挥其抗炎作用.
CEP显示出作为类风湿性关节炎 (RA) 的补充或替代治疗剂的巨大潜力.

关键词:

塞法兰提因是一种素.糖溶性新陈代谢的发生.巨细胞的两极分化一个单细胞单细胞.类风湿性关节炎类风湿性关节炎类风湿性关节炎

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