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阿司匹林和切莱科西布调节Notch1/Hes1通路,防止压力过载诱导的心肌缩

Minghui Wei¹, Ziyu Lu¹, Haifeng Zhang²

¹School of Basic Medicine, Inner Mongolia Medical University.

International heart journal

|June 2, 2024

概括

像阿司匹林这样的循环氧化酶 (COX) 抑制剂可能会保护心脏免受缩和炎症. 这些保护作用似乎与Notch1/Hes1信号通路的激活有关.

科学领域:

心血管生物学心血管生物学
分子医学是分子医学.
药理学药理学是指药理学的学科.

背景情况:

心肌缩是心血管疾病的重要危险因素.
炎症在心脏缩和功能障碍的进展中起着至关重要的作用.
关联炎症和缩的分子机制需要进一步阐明.

研究的目的:

调查循环氧化原酶 (COX) 抑制剂对心肌缩的保护机制.
探索Notch1/Hes1信号通路在COX抑制剂介导心脏保护中的作用.
评估COX抑制剂对炎症和缩标志物的影响在体外和体内.

主要方法:

在SD大鼠中通过横向大动脉收缩诱导心肌缩,在H9c2心肌细胞中通过机械拉伸诱导心肌缩.
心声图和尾部动脉压测量以评估心脏功能.
定量PCR (qPCR) 和西部抹黑来分析与Notch相关的信号 (Notch1,Hes1) 表达.
在血清,心脏组织和细胞培养中量化炎症性细胞因子 (IL-6,TNF-α,IL-1β,IL-10) 的ELISA.

主要成果:

压力过重和机械拉伸导致心肌缩,炎症和纤维化,伴随着减少Notch1和Hes1的表达.
治疗COX抑制剂 (阿司匹林,切莱科克西布) 改善了缩,纤维化和炎症.
服用COX抑制剂导致Notch1/Hes1通路的激活,与心脏功能改善和炎症减少相关.
在体外,机械拉伸增加了炎症和缩标志物,同时降低了Notch1/Hes1;COX抑制剂逆转了这些效应.

结论:

COX 抑制剂显示出对心肌缩和炎症的保护作用.
诺奇1/Hes1信号通路与COX抑制剂的心脏保护机制有关.
准Notch1/Hes1通路可能是治疗心脏缩和炎症的治疗策略.

关键词:

循环氧化基因酶 (Cyclooxygenase) 是一种炎症炎症是一种炎症.缺口信号通道的信号通道.

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