Exploration of a novel role for lidocaine as a wide range spectrum anti-infection drug

恶性疟原虫（疟疾的病原体）和猫免疫缺陷病毒（猫免疫缺陷病毒）分别作为寄生虫和病毒感染的模型。利多卡因治疗破坏了宿主细胞中的脂筏，同时抑制了寄生虫的入侵和病毒的进入。详细的研究表明，疟疾寄生虫激活了在宿主红细胞中介导的信号转导，从而磷酸化了一种膜骨架蛋白——失钙蛋白。失活蛋白的磷酸化导致膜骨架网的短暂松动，允许寄生虫入侵。利多卡因被证明可以通过破坏脂筏来防止膜骨骼松动，从而抑制寄生虫的入侵

Plasmodium falciparum, a causative agent of malaria, and feline immunodeficiency virus were used as models for parasitic and viral infection, respectively. Lidocaine treatment disrupted lipid rafts in respective host cells and concomitantly inhibited the parasite invasion and viral entry. Detailed study revealed that malaria parasites activateraft-mediated signal transduction in host erythrocytes to phosphorylate dematin, a membrane skeletal protein. Phosphorylation of dematin results in a transient loosening of membrane skeletal meshwork, allowing the parasite invasion. Lidocain was shown to inhibit the parasite invasion by preventing membrane skeletal loosening via disruption of lipid rafts