Toxoplasma gondii (T. gondii) is an important health problem in human and animals, and the highlighting side effects of launched therapeutic chemicals cannot be ignored. Thus, it is urgent to develop new drugs to against the infection. Myrislignan originated from nutmeg exhibited excellent anti-T. gondii activity in vitro and in vivo, and was able to destroy mitochondrial function. However, the exact mechanism of action is still unknown. In this study, combining RNAs deep-sequencing analysis and surface plasmon resonance (SPR) analysis, the differentially expressed genes (DEGs) and high affinity proteins suggested that myrislignan may affect the oxidation-reduction process of T. gondii. Furthermore, the upregulating ROS activity after myrislignan incubation verified that myrislignan destroyed the oxidant-antioxidant homeostasis of tachyzoites. Transmission electron microscopy (TEM) indicated that myrislignan induced the formation of autophagosome-like double-membrane structure. Moreover, monodansyl cadaverine (MDC) staining and western blot further illustrated autophagosome formation. Myrislignan treatment induced a significant reduction in T. gondii by flow cytometry analysis. Together, these findings demonstrated that myrislignan can induce the oxidation-reduction in T. gondii, lead to the autophagy, and cause the death of T. gondii.

中文翻译：

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Myrislignan 在弓形虫中诱导氧化还原失衡并激活自噬。

弓形虫 (T. gondii) 是人类和动物的重要健康问题，发射的治疗性化学品的突出副作用不容忽视。因此，迫切需要开发新的抗感染药物。源自肉豆蔻的 Myrislignan 表现出优异的抗 T。体外和体内的弓形虫活性，并能够破坏线粒体功能。然而，确切的作用机制仍然未知。在这项研究中，结合RNAs深度测序分析和表面等离子体共振（SPR）分析，差异表达基因（DEGs）和高亲和力蛋白表明肉豆蔻木脂素可能影响弓形虫的氧化还原过程。此外，肉豆蔻木脂素孵育后 ROS 活性的上调证实肉豆蔻木脂素破坏了速殖子的氧化-抗氧化稳态。透射电子显微镜 (TEM) 表明，肉豆蔻木脂素诱导自噬体样双膜结构的形成。此外，单丹糖尸胺 (MDC) 染色和蛋白质印迹进一步说明了自噬体的形成。通过流式细胞术分析，肉豆蔻木脂素处理诱导了弓形虫的显着减少。总之，这些发现表明，肉豆蔻木脂素可以诱导弓形虫的氧化还原，导致自噬，并导致弓形虫死亡。