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酸调解了GPR84依赖和独立的保护,防止败血症引起的心肌功能障碍

Yao Lin¹, Wenbin Zhang¹, Xiangkang Jiang¹

¹Department of Emergency Medicine, Second Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou 310009, China; Key Laboratory of The Diagnosis and Treatment of Severe Trauma and Burns of Zhejiang Province, Hangzhou 310009, China; Clinical Research Center for Emergency and Critical Care Medicine of Zhejiang Province, Hangzhou 310009, China.

Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie

|September 28, 2024

概括

乙酸 (SO) 通过通过G蛋白结合受体84 (GPR84) 减少炎症和氧化应激,防止败血症引起的心肌功能障碍 (SIMD). 此外,SO还可以增强心脏能量代谢,可能是通过中链乙-CoA脱酶 (MCAD).

科学领域:

心血管研究研究心血管研究
败血症病理生理学病理生理学
分子药理学分子药理学

背景情况:

败血症诱导的心肌功能障碍 (SIMD) 是败血症的一个关键并发症.
鉴定SIMD的有效治疗剂仍然是一个重大的临床挑战.

研究的目的:

在SIMD.的小鼠模型中研究酸 (SO) 的治疗潜力.
阐明SO的保护作用的基础分子机制,包括它与G蛋白结合受体84 (GPR84) 的相互作用以及它对心脏能量代谢的影响.

主要方法:

在雄性小鼠中使用脂聚糖 (LPS) 和结和穿孔 (CLP) 建立了败血症模型.
八酸盐 (SO) 在败血症诱导后的不同间隔内被施用.
通过GEO数据分析,分子对接和使用DBA/2小鼠的实验来评估GPR84的参与.
用代谢学分析心脏能量代谢.
在SO治疗的败血症小鼠的心脏中发现了基斯修饰.

主要成果:

SO治疗显著改善了心肌收缩功能,并减少了氧化应激.
施用SO提高了GPR84的表达,而GPR84的缺乏减弱了SO的保护作用.
通过促进乙-CoA合成和脂肪酸β-氧化,SO增强了心肌能量代谢,影响取决于中链乙-CoA脱酶 (MCAD).
由SO诱导的素乙化,特别是在H3K123和H3K80.0.

结论:

八酸 (SO) 提供对败血症诱导的心肌功能障碍 (SIMD) 的保护.
SO的保护机制包括GPR84介导的抗炎/抗氧化作用和GPR84独立的心脏能量代谢增强,可能通过MCAD.
这些发现凸显了SO作为SIMD的潜在治疗候选者.

关键词:

能量代谢能量代谢在 GPR84 中使用.在MCAD中,我们可以使用MCAD.氧化应激是一种氧化应激.败血症引起的心肌功能障碍八酸盐是一种酸盐.

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