Tuftsin修饰阿魏酸调控“Autophagy-Ferroptosis”信号通路靶向增强抗PPV作用机制研究

猪细小病毒（Porcine parvovirus,PPV）感染宿主诱导细胞自噬发生且与细胞凋亡有着密切联系。前期研究发现阿魏酸（Ferulic Acid,FA）通过调控BID-线粒体凋亡信号通路发挥抗PPV作用，且阿魏酸调控自噬过程的发生发挥保护细胞的作用。阿魏酸中兽医临床应用存在诸多限制，纳米药物多用来解决该问题。研究表明，促吞噬肽（Tuftsin）修饰阿魏酸纳米粒子有效改善药物稳定性及靶向性增强抗PPV作用。本研究采用W/O/W制备阿魏酸纳米粒（FA NPs），促吞噬肽进一步修饰FA NPs制备TF-FA NPs，研究其结构特征；探究TF-FA NPs调控“Autophagy-Ferroptosis”进一步发挥抗PPV的作用机制；明确TF-FA NPs调控P53/BH3结构域相关信号分子进一步促进Autophagy-Ferroptosis的分子机理，为抗病毒药物的研究提供科学依据。

Porcine parvovirus (PPV) infection induces autophagy and is closely related to apoptosis.Ferulic Acid (FA) plays an anti-ppv role by regulating the bid-mitochondrial apoptosis signaling pathway, and Ferulic Acid plays a protective role in regulating the occurrence of autophagy.There are some disadvantages,such as drug instability and low biological activity,in Chinese veterinary clinic.Currently,nanomaterials are widely used in Chinese veterinary medicine,due to small particles, high surface reactivity and excellent stability.In our previous study,tufsin modified ferulic acid nanoparticles can effectively improve drug stability and enhance anti-ppv targeting.In this study, ferulic acid nanoparticles (FA NPs) were prepared by W/O/W, and further modified by Tuftsin to prepare TF-FA NPs.To explore the mechanism of TF-FA NPs regulating "autophagy-ferroptosis" to further play the role of anti-ppv.The molecular mechanism of autophagy-ferroptosis is further enhanced by the regulation of P53/BH3 domain by tf-fa NPs, which provides scientific basis for the study of antiviral drugs.