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Updated: Feb 7, 2026

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Whole Mount Immunohistochemistry in Zebrafish Embryos and Larvae
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酸通过调节斑马鱼胚胎幼虫的炎症反应和痕信号来保护LPS诱导的心脏功能障碍
Modi Kiran Piyushbhai1, Ambika Binesh1, Kaliyamurthi Venkatachalam1
1Institute of Fisheries Post Graduate Studies, Tamil Nadu Dr. J. Jayalalithaa Fisheries University (TNJFU), OMR Campus, Vaniyanchavadi, Chennai, India.
Journal of biochemical and molecular toxicology
|February 5, 2026
概括
酸 (GA) 通过抑制Notch信号通路,保护斑马鱼的心脏免受脂聚糖 (LPS) 造成的损伤. 这种天然化合物通过减少炎症和改善心脏功能来提供心血管益处.
科学领域:
- 心血管研究研究心血管研究
- 分子生物学分子生物学
- 药理学 药理学是指药理学的学科.
背景情况:
- 心血管疾病对全球健康构成重大威胁,需要对有效的预防剂进行研究.
- 酸 (GA) 是一种天然的多,具有潜在的心脏保护性质,但其潜在的机制尚不清楚.
- 诺奇信号通路在心脏损伤和修复过程中起着至关重要的作用.
研究的目的:
- 在Lipopolysaccharide (LPS) 诱导的斑马鱼胚胎幼虫 (ZFEL) 模型中研究酸 (GA) 的心脏保护作用.
- 阐明Notch信号通路在调解GA的心脏保护活性中的作用.
主要方法:
- 在ZFEL中使用LPS诱导建立了体内心脏损伤模型.
- 通过生存分析,形态评估,心率监测,细胞死亡试验和氧化测定来评估GA的心脏保护功效.
- 分析了Notch信号元件 (Notch1,Delta1,Hey1,Hes1) 和心脏生物标志物 (MPO,MMP-9,MMP-13,NO) 的表达水平,使用免疫栓塞和免疫组织化学.
主要成果:
- 在LPS治疗的ZFEL中,酸显著改善了生存率,心脏形态和心脏率正常化,减少了细胞死亡,并抑制了氧化生成.
- GA治疗抑制了Notch信号通路的激活,包括Notch1,Delta1,Hey1和Hes1等关键蛋白质.
- 心脏损伤标志物的表达,包括骨髓氧化酶 (MPO),矩阵金属蛋白酶-9 (MMP-9),矩阵金属蛋白酶-13 (MMP-13) 和氧化 (NO),由GA降低调节.
结论:
- 酸在斑马鱼胚胎中显示出显著的心脏保护作用,防止LPS诱导的心脏损伤.
- GA的心脏保护机制涉及抑制Notch信号通路.
- 这些发现突出了GA作为一种潜在的治疗药物,用于心血管保护,通过调节Notch信号来调节.
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