昆塞诺化物通过通过TLR4/STAT1信号通路抑制M1巨细胞极化来缓解实验性急性胰腺炎

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Ruiyan Wang¹, Jing Jiang¹, Pengli Song¹

¹Department of Gastroenterology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China; Shanghai Key Laboratory of Pancreatic Disease, Institute of Pancreatic Disease, Shanghai Jiao Tong University School of Medicine, Shanghai, China.

Journal of ethnopharmacology

|February 25, 2025

概括

昆塞诺 (KD) 通过减少炎症和M1巨分化,有效治疗急性胰腺炎 (AP). 这种天然化合物显示出通过TLR4/STAT1通路管理AP的前景.

科学领域:

药理学药理学是指药理学的学科.
免疫学免疫学免疫学
胃肠病学胃肠病学

背景情况:

急性胰腺炎 (AP) 是一种严重的炎症状况,有可能损害多个器官.
基因化物 (KD) 是从Anoectochilus roxburghii中提取的,具有抗炎和免疫调节的特性.
在AP中KD的治疗潜力以前没有被探索.

研究的目的:

研究KD对急性胰腺炎 (AP) 的保护作用.
阐明KD在AP中的作用背后的分子机制.

主要方法:

建立了两种AP的小鼠模型 (素/LPS和陶酸盐).
通过组织病理学和血清标志物进行KD前期治疗和评估AP严重程度.
使用免疫光学,流细胞计和qRT-PCR分析了巨细胞透和表型.
利用网络药理学和转录基因测序来识别KD标和途径,通过qPCR和Western blot进行验证.

主要成果:

在AP模型中,KD (10 mg/kg) 显著降低了胰腺损伤,,缩和炎症细胞透.
凯迪的使用降低了血清脂酶和粉酶水平,并减轻了全身炎症和肺损伤.
在体外,KD (400μM) 抑制了M1巨分化,并降低了M1相关基因表达的调节.
确定KD向TLR4,抑制巨细胞中的TLR4/STAT1信号通路.

结论:

通过TLR4/STAT1通路抑制M1巨细胞极化,KD可以缓解实验性AP.
这些发现确立了KD作为治疗急性胰腺炎的潜在治疗剂.

关键词:

在急性胰腺炎中,这是一种昆塞诺化物.在M1极化中,M1极化巨细胞是一个巨细胞.在TLR4/STAT1中.

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