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一种草药配方的沈莲可以通过抑制补体级联来调节肝细胞癌中M1/M2巨的比例

Wenxuan Li¹, Liping You¹, Jiacheng Lin²

¹Department of Liver Diseases, Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai, China; Central Laboratory, Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai, China.

Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie

|June 15, 2024

概括

沈莲 (SLD) 通过减少免疫抑制来对抗肝细胞癌 (HCC). 它的目标是补充C5信号,增强抗瘤免疫力,并为HCC提供潜在的草药疗法.

科学领域:

免疫学免疫学免疫学
在瘤学瘤学.
药理学药理学是一个学科.

背景情况:

瘤微环境显著影响肝细胞癌 (HCC) 的进展.
对HCC的有效治疗方法仍然有限,这凸显了对新型治疗策略的需求.
沈莲 (SLD) 是一种已注册的治疗HCC的草药疗法,但其机制尚不清楚.

研究的目的:

在肝细胞癌 (HCC) 中研究沈莲 (SLD) 的抗瘤作用.
阐明SLD发挥治疗作用的潜在分子机制.

主要方法:

使用各种方法 (β-catenin/C-Met,DEN/CCl4) 诱导的HCC的小鼠模型.
通过肝脏重量和组织学分析评估瘤生长.
分析瘤透免疫细胞使用流动细胞计和免疫染色.
采用非向蛋白质组学来识别分子点,并在共同培养系统中验证了发现.

主要成果:

SLD显著抑制了HCC的进展和瘤的生长.
SLD促进了巨细胞的透,并将M1/M2巨细胞比率转移到抗瘤表型.
蛋白质组分析显示,SLD的关键机制涉及抑制补体C5 / C5a信号传递.
SLD抑制了C5/C5a表达和C5aR1+巨细胞的透,其效果被C5aR1抑制剂模仿.
SLD直接准肝瘤细胞,防止由瘤细胞超标诱导的巨细胞的M2极化.
SLD抑制了参与C5转录的上游AMPK/p38信号通路.

结论:

沈莲 (SLD) 通过抑制C5表达来缓解HCC中的免疫抑制性瘤微环境.
通过抑制AMPK/p38信号传递,SLD抑制了肝瘤细胞中的C5分泌.
通过调节免疫格局,SLD代表了对HCC的有希望的草药治疗策略.

关键词:

补充级联是补充级联.肝细胞癌是肝细胞癌.在 SLD 和 SLD 之间.与瘤相关的巨细胞.

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