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马格诺洛尔作为治疗多发性硬化症的STAT3抑制剂,通过限制Th17细胞来治疗多发性硬化症

Jian-Yu Chen¹, Xiao-Yun Tian¹, Shan-Shan Wei²

¹Department of Pharmacology, School of Pharmacy, Fujian University of Traditional Chinese Medicine, No.1, Hua Tuo Road, Min Hou Shang Jie, Fuzhou 350122, China.

Phytomedicine : international journal of phytotherapy and phytopharmacology

|June 10, 2023

概括

马格诺洛尔 (Magnolol) 是一种来自马格诺利亚植物 (Magnolia officinalis) 的化合物,通过通过STAT3信号来抑制Th17细胞分化和IL-17A表达,有效治疗多发性硬化症 (MS). 这表明它有可能成为MS的新型治疗剂.

科学领域:

神经免疫学神经免疫学
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:

多发性硬化症 (MS) 是一种由Th17细胞驱动的中枢神经系统免疫疾病.
信号转换器和转录3激活器 (STAT3) 在MS中促进Th17分化和IL-17A产生.
马格诺洛尔 (Magnolol) 是由马格诺利亚花 (Magnolia officinalis) 衍生而来的,目前正在作为一种潜在的MS治疗药物进行研究.

研究的目的:

为了评估magnolol在治疗实验性自身免疫脑膜炎 (EAE) 的疗效,MS的小鼠模型.
阐明magnolol影响Th17细胞分化和STAT3信号的体外和体外机制.

主要方法:

在小鼠体内EAE模型以评估magnolol的治疗效果.
在体外FACS测定Th17/Treg细胞分化和IL-17A表达.
网络药理学,西部抹杀,SPR和分子对接,以调查magnolol与JAK/STAT通路的相互作用,特别是STAT3.

主要成果:

马格诺洛尔减轻了EAE症状,减少了脊髓病变,并在体内减少了炎症细胞透和细胞因子水平.
马格诺洛尔在体外选择性地抑制了Th17分化和IL-17A的产生,而不会影响Treg细胞.
发现马格诺洛尔可以抑制STAT3酸化,核转位和转录活性,对STAT3有很高的亲和力,这表明STAT3是其主要目标.

结论:

马格诺洛尔通过通过STAT3阻断选择性抑制Th17分化和IL-17A表达来证明MS的治疗潜力.
这种机制降低了Th17/Treg细胞比率,将马格诺洛尔定位为MS治疗的有前途的新型STAT3抑制剂.

关键词:

这是一种磁醇.多发性硬化症 (MS) 是一种疾病.时间时间时间信号传感器和转录3 (stat3) 的激活器 Th17 这是一个很好的方法.

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