再组合的HALT-1在HeLa细胞中诱导线粒体相关的亡机制
Lok Wenn Loo1, Jung Shan Hwang2
1Department of Biomedical Sciences, Sir Jeffrey Cheah Sunway Medical School, Faculty of Medical and Life Sciences, Sunway University, No. 5, Jalan Universiti, 47500, Bandar Sunway, Selangor Darul Ehsan, Malaysia.
Scientific reports
|December 11, 2025
概括
类似于Hydraactinoporin的毒素-1 (HALT-1) 通过线粒体通路诱导HeLa细胞的亡. 这种形成孔隙的毒素通过改变线粒体膜潜力和亡蛋白表达来触发细胞死亡,独立于活性caspase-3.
科学领域:
- 细胞生物学 细胞生物学
- 毒理学 毒理学 毒理学
- 生物化学 生物化学
背景情况:
- 酸乙烯类毒素-1 (HALT-1) 是来自Hydra magnipapillata的一种α-PFT (α-孔形成毒素).
- 虽然HALT-1的细胞毒性和溶血性质已知,但其精确的亡机制和细胞信号通路仍未得到充分探索.
- 之前的研究证实了HALT-1的剂量依赖性细胞毒性 (CC50 = 15.4μg/mL).
研究的目的:
- 研究HALT-1在HeLa细胞中诱导的亡机制和细胞信号通路.
- 阐明线粒体通路和体在HALT-1介导的细胞死亡中的作用.
主要方法:
- 实时Annexin V和DNA染料测试以评估亡和亡.
- 流细胞计分析线粒体膜潜力.
- 西部斑点分析用于检查与亡相关的蛋白质的表达 (例如,Bad,Bax,BCL-2,BCL-xL,caspases).
主要成果:
- rHALT-1 (12微克/毫升) 诱导了剂量和时间依赖的亡,在7小时达到峰值,亡最小.
- 在没有活性caspase-3的情况下观察到线粒体膜潜在脱极化.
- 检测到对亲亡蛋白质 (Bad,Bax,cytochrome c,caspase-9) 的上调和对抗亡蛋白质 (Bcl-2,Bcl-xL) 的下调.
结论:
- HALT-1主要通过线粒体通路诱导HeLa细胞的亡.
- HALT-1诱导的亡的执行阶段似乎不涉及活性caspase-3.
- 结果提供了关于HALT-1的作用机制和在毒素研究中的潜在应用的见解.
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