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胃素通过降低巨细胞中TLR4表达的调节来减轻败血症引起的心肌功能障碍

Dandong Fang^1,2,3, Yu Li^1,2, Bo He^1,2

¹Department of Cardiology, Daping Hospital, the Third Military Medical University (Army Medical University), Chongqing 400000, China.

Acta pharmaceutica Sinica. B

|September 18, 2023

概括

胃蛋白通过激活其受体CCKBR.通过激活其受体在败血症期间保护心脏. 这种机制涉及减少炎症和巨细胞透,为败血症引起的心肌功能障碍提供潜在的新疗法.

科学领域:

心脏病学心脏病学
免疫学免疫学免疫学
胃肠病学胃肠病学

背景情况:

败血症引起的心肌功能障碍 (SMD) 是一个关键的并发症.
胃肠功能障碍和SMD之间的联系尚未完全理解.

研究的目的:

调查胃素及其受体 (CCKBR) 在败血症引起的心肌功能障碍中的作用.
阐明素在SMD中的保护作用的潜在机制.

主要方法:

评估了SMD和没有SMD的患者的血胃素水平.
使用了毒症 (LPS诱导的心脏功能障碍) 的小鼠模型.
操纵CCKBR表达和胃素水平,以及耗尽的巨细胞.

主要成果:

在SMD患者中血胃素的升高.
在小鼠中,CCKBR缺陷加剧了LPS诱导的心脏功能障碍和炎症.
施用Gastrin改善了心脏病和心脏损伤.
大细胞枯竭和CCKBR过度表达的BMM减少了心脏损伤.
胃素通过巨细胞的PPAR-α通路抑制TLR4的表达.

结论:

加斯特林通过CCKBR起作用,对SMD产生保护作用.
胃素/CCKBR通路调节心脏炎症和巨细胞在败血症中的反应.
这一途径为SMD治疗提供了潜在的治疗点.

关键词:

胆固醇托基宁B受体的受体胃肠是指胃的内脏.炎症炎症是一种炎症.脂聚糖类糖化物脂聚糖类糖化物巨细胞是一个巨细胞.过氧体增殖器激活的受体α.败血症引起的心肌功能障碍收费类受体4 收费类受体4

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