甲基苯丙胺与HIV-1 Tat蛋白单独及协同诱导神经炎症机制的研究进展

Research progress on mechanisms of neuroinflammation induced by methamphetamine and HIV-1 Tat protein

甲基苯丙胺(methamphetamine,METH)滥用和人类免疫缺陷病毒(human immunodeficiency virus,HIV)感染是当今世界面临的极其严重的公共卫生和社会问题。METH与HIV-1 Tat蛋白可单独及协同诱导神经毒性,而神经炎症是引起神经毒性的重要机制之一。神经炎症可由神经胶质细胞、细胞因子、NLRP3炎性小体等介导调控。该文综述了近年来METH与HIV-1 Tat蛋白单独及协同诱导神经炎症机制的研究进展,旨在为将来进一步探索两者协同诱导神经炎症的机制以及有效的药物干预靶点提供参考和依据。

Methamphetamine abuse and HIV infection are extremely serious public health and social problems facing the world today.Methamphetamine and HIV-1 Tat protein can induce neurotoxicity in an individual and synergistic way,and neuroinflammation is one of the most important mechanisms for ca-using neurotoxicity.Neuroinflammation can be mediated by glial cells,cytokines,NLRP3 inflammasomes,etc.This paper reviews the research progress of neuroinflammation induced by methamphetamine and HIV-1 Tat protein in recent years,with the aim of providing reference and basis for further exploration of the mechanisms of neuroinflammation caused by them and effective drug intervention targets in the future.