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miR-361-5p通过调解SLPI/ NF-κB信号通路来调节急性感染性内心炎

Hua Li^1,2,3,4, Yaxiong Li^1,2,3,4, Shen Han^1,2,3,4

¹Department of Cardiovascular Surgery, Yan'an Hospital Affiliated to Kunming Medical University, No.245 Renmin East Road, Kunming, 650051 Yunnan China.

|August 25, 2025

概括

通过增加分泌白细胞蛋白酶抑制剂 (SLPI) 和抑制NF-κB通路,降低miR-361-5p对急性传染性内心炎 (AIE) 的保护作用. 这一发现为AIE治疗提供了新的治疗策略.

科学领域:

心血管生物学
分子医学
传染性疾病

背景情况:

急性传染性内心炎 (AIE) 涉及内心炎症和植被形成,通常与金黄色葡萄球菌 (SA) 感染有关.
微RNA-361-5p (miR-361-5p) 和分泌白细胞蛋白酶抑制剂 (SLPI) 在AIE病变发生过程中的具体作用在很大程度上尚未确定.
肺炎感染和缺氧是AIE发展的关键因素,影响心脏细胞和功能.

研究的目的:

阐明 miR-361-5p 和 SLPI 在 Staphylococcus aureus 引起的急性感染性内心炎中的功能作用和分子机制.
研究miR- 361-5p与SLPI之间的相互作用以及它们对心脏细胞活力,细胞亡和炎症反应的联合作用.
在已建立的AIE模型中评估调节miR-361-5p水平的治疗潜力.

主要方法:

使用受低氧和SA感染的AC16细胞建立AIE细胞模型,以及AIE大鼠模型.
双露西法酶测定证实了miR-361-5p和SLPI之间的向相互作用.
定量评估包括RT-qPCR,西部抹血,CCK-8,流细胞测量,ELISA,H&E染色和TUNEL染色以分析分子和细胞变化.

主要成果:

在AIE模型中,miR-361-5p是上调的,而SLPI是下调的;miR-361-5p直接针对SLPI.
在体外,miR- 361-5p促进了细胞亡和炎症 (CK- MB,cTnT,IL- 1β,TNF- α的升高) 并激活了NF- kB p65信号,而SLPI过度表达或miR- 361-5p倒置则逆转了这些效应.
在体内,miR-361-5p降低了AIE大鼠的膜植被,心肌亡和心脏损伤标志物.

结论:

通过上调SLPI和抑制NF-κB p65信号通路,对miR-361-5p的下调具有保护作用.
miR-361-5p/SLPI轴代表了AIE病变的关键调节机制.
针对miR-361-5p为治疗急性传染性内心炎提供了一个有前途的治疗策略.

关键词:

急性感染性内心炎细胞活力分泌白细胞蛋白酶抑制剂黄金葡萄球菌 miR-361-5p的使用情况

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