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沉默miR-155-5p表达通过抑制死性肠球炎的炎症和铁亡来改善肠损伤

Le Zhang^1,2, Weilai Jin², Mengyuan Hu³

¹Key Laboratory of Birth Defects, Children's Hospital, Institutes of Biomedical Sciences, Fudan University, Shanghai, China.

|September 17, 2024

概括

减少miR-155-5p的表达可以通过抑制炎症和铁亡来缓解死性肠球炎 (NEC) 中的肠损伤. 这为NEC治疗提供了潜在的新治疗策略.

科学领域:

生物医学科学生物医学科学
分子生物学分子生物学
胃肠病学胃肠病学

背景情况:

死性肠球炎 (NEC) 是一种严重的肠道疾病,主要影响早产婴儿.
在NEC肠道组织中观察到miR-155-5p的表达增加,但其作用和机制尚不清楚.

研究的目的:

研究miR-155-5p在NEC病原发生中的作用.
阐明涉及NEC中miR-155-5p的潜在分子机制.

主要方法:

建立了体外 (脂聚糖诱导) 和体内 (低氧和配方养) 的NEC模型.
评估了炎症性细胞因子,细胞存活率,细胞亡,氧化应激标志物 (GSH,SOD,CAT,MDA),ROS,线粒体膜潜力和与铁亡相关的蛋白质.
使用西式涂抹和血素和氨酸染色用于分子和本病理学分析.

主要成果:

在NEC模型中,抑制miR-155-5p改善了细胞存活率,减少了细胞亡,炎症和铁亡.
miR-155-5p直接向SLC7A11;其抑制上调SLC7A11,减轻LPS诱导的炎症和铁亡.
观察到铁亡标记物 (FTH1,GPX4,COX-2,ACSL4),氧化应激标记物,炎症性细胞因子 (IL-6,TNF-α) 和抑制的IκBα/NF-κB p65信号的变化.

结论:

减少miR-155-5p的表达,通过抑制炎症和铁亡,改善了NEC的肠损伤.
向miR-155-5p为NEC提供了一个有希望的治疗途径,得到了SLC7A11调节的机制性见解的支持.

关键词:

铁化是铁化的一种.炎症炎症是一种炎症.在MiR-1555p中使用.死性肠道结肠炎 (NECO) 是一种

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