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石康宁通过调节PKM2来抑制免疫检查点PD-L1在败血症中巨细胞的表达

Lijia Yuan¹, Yong Wang², Youlian Chen³

¹Department of Critical Care Medicine, Shenzhen People's Hospital, First Affiliated Hospital of Southern University of Science and Technology, Second Clinical Medicine College of Jinan University, Shenzhen 518020, China; Department of Traditional Chinese Medicine, Integrated Chinese and Western Medicine Postdoctoral Research Station, Jinan University, 601 Huangpu Road, Guangzhou 510632, China.

International immunopharmacology

|June 11, 2023

概括

希科宁是一种天然化合物,有效地减少了小鼠的败血症引起的炎症和免疫抑制. 它降低了促炎性细胞因子,并通过向pyruvate kinase M2 (PKM2) 来降低编程死亡配体1 (PD-L1) 的表达.

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.
分子生物学分子生物学

背景情况:

败血症是一种全球性健康危机,由于免疫系统失调和缺乏有效治疗方法,死亡率高.
编程死亡配体1 (PD-L1) 通过促进免疫抑制来加剧败血症,但其精确的调节机制尚不清楚.
石康宁是一种传统中医药成分,具有抗炎和减轻败血症的特性.

研究的目的:

为了研究shikonin在败血症中的治疗潜力.
阐明石康宁对PD-L1表达的作用及其与酸盐激酶M2 (PKM2) 在败血症中的相互作用.

主要方法:

在使用脂聚糖 (LPS) 的小鼠模型中诱导了败血症.
评估了什科宁对炎症性细胞因子,T细胞百分比和细胞亡的作用.
在活体和体外分析了巨细胞上的PD-L1表达和T细胞上的PD-1.
研究了康宁,PKM2和PD-L1促进体之间的相互作用.

主要成果:

在败血症小鼠中,西康宁显著降低了炎症性细胞因子 (TNF-α,IL-6,IFN-γ,IL-1β) 的血清水平.
什科宁维持了T细胞百分比,并减少了LPS诱导的败血症中的脊髓细胞亡.
石康宁降低了巨细胞上的PD-L1表达,但没有降低T细胞上的PD-1.
石康宁通过降低PKM2酸化和核进口的调节来减弱PD-L1表达,抑制PKM2与PD-L1促进物结合.

结论:

石康宁通过减轻炎症和免疫抑制,在败血症小鼠模型中显示出显著的治疗益处.
石康宁的机制涉及通过PKM2通路对巨细胞上PD-L1表达的下调.
需要进一步的临床研究来验证Shikonin在通过向PKM2-介导的PD-L1调节来治疗败血症的疗效.

关键词:

巨细胞是一个巨细胞.在PD-L1中.在PKM2中,PKM2是PKM2.败血症这是一种败血症.在西康尼尼 (Shikonin) 书房里.

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