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佩拉戈尼 (Pelargonium sidoides) 提取物通过线粒体功能障碍和细胞骨不稳定性来调解毒性

Ju Young Lee¹, JuKyung Lee², Sung Ho Lee³

¹Animal Model Research Group, Korea Institute of Toxicology, 30 Baekhak1-gil, Jeongeup, Jellabuk-do 56212 Republic of Korea.

Toxicological research

|October 2, 2023

概括

佩拉戈尼 (Pelargonium sidoides) 提取物通过破坏线粒体和破坏细胞骨架来诱导细胞的细胞死亡. 这一过程涉及增加的活性氧物种和亡信号,这表明其细胞毒性作用的潜在机制.

科学领域:

细胞生物学细胞生物学
药理学药理学是指药理学的学科.
毒理学毒理学毒理学

背景情况:

佩拉戈尼 (Pelargonium sidoides) 是一种具有已知的治疗功能的药用植物.
了解其细胞毒性机制对于其安全有效的使用至关重要.

研究的目的:

为了研究Pelargonium sidoides提取物对马丁-达比犬 (MDCK) 细胞的细胞毒性作用.
阐明P. sidoides诱导的细胞毒性背后的分子机制,重点关注线粒体功能,细胞亡和细胞骨完整性.

主要方法:

进行了细胞活力测试,以评估P. sidoides提取物的剂量依赖性细胞毒性作用.
测量了线粒体膜潜力,反应性氧物种 (ROS) 水平和尼古丁胺胺氨基二核酸化物 (NADH) 释放.
使用mRNA测序和免疫块分析来研究与亡相关的基因表达和亡信号通路中的蛋白质水平.
使用N-乙-L-氨酸 (NAC) 预处理,研究了ROS的参与.
分析了小GTPase活性 (RhoA,Rac1/cdc42) 和相关的细胞骨信号通路.
在与NAC或RhoA/Rac1/cdc42激活剂预处理或不进行P. sidoides提取物治疗后,评估了动氨酸细胞骨稳定性.

主要成果:

P. sidoides提取物以剂量依赖的方式降低了MDCK细胞活力.
提取物诱导了线粒体功能障碍,其证据是线粒体作用潜能降低,ROS增加和NADH释放.
mRNA测序揭示了与亡相关的基因BBC3的上调,进一步通过显示亡标记物 (Bcl-2,Bax,CytC,caspases,PARP) 调节的免疫块分析得到证实.
ROS调解了观察到的亡,这是通过抑制NAC预处理的亡标志物所证明的.
P. sidoides提取物抑制了RhoA和Rac1/cdc42的活性,导致细胞骨相关的信号蛋白的下游抑制和actin不稳定.
NAC或RhoA/Rac1/cdc42激活剂预处理抵消了P. sidoides提取物诱导的actin不稳定.

结论:

P. sidoides 提取物通过诱导线粒体功能障碍和细胞骨架分解,对MDCK细胞产生细胞毒性作用.
提取物促进了亡,这是一个由ROS生产显著影响的过程.
抑制RhoA和Rac1/cdc42信号通路在提取物对细胞骨和整体细胞毒性的影响中起着关键作用.

关键词:

细胞灭亡 (apoptosis) 是一种死亡的过程.细胞骨架细胞骨架皮拉戈尼乌姆 (Pelargonium sidoides) 的提取物是可以提取的.这就是ROSOS ROS.

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