Department of Neurology, Sun Yat-sen Memorial Hospital of Sun Yat-sen University, Guangzhou 510120, People's Republic of China.
Neurol Sci. 2013 Feb;34(2):137-41. doi: 10.1007/s10072-012-1156-0. Epub 2012 Jul 21.
Rifampicin is a macrocyclic antibiotic used extensively for the treatment of Mycobacterium tuberculosis and other mycobacterial infections. Recently, it was discovered that rifampicin exhibits neuroprotective effects. It has been shown to protect PC12 cells against MPP(+)-induced apoptosis and inhibit the expression of α-synuclein multimers. In in vitro studies, rifampicin pretreatment protects PC12 cells against rotenone-induced cell death. Qualitative and quantitative analyses uncover that rifampicin significantly suppresses rotenone-induced apoptosis by ameliorating mitochondrial oxidative stress. It reduces microglial inflammation and improves neuron survival. Our results indicate that rifampicin is cytoprotective under a variety of experimental conditions, and suggest that it may be useful in PD therapeutics. It is the aim of this paper to review the experimental neuroprotection data reported using rifampicin with a focus on the molecular and cellular mechanisms of cytoprotective effect in in vitro models of PD.
利福平是一种广泛用于治疗结核分枝杆菌和其他分枝杆菌感染的大环内酯类抗生素。最近发现,利福平具有神经保护作用。它已被证明可以保护 PC12 细胞免受 MPP(+)诱导的细胞凋亡,并抑制α-突触核蛋白多聚体的表达。在体外研究中,利福平预处理可保护 PC12 细胞免受鱼藤酮诱导的细胞死亡。定性和定量分析揭示,利福平通过改善线粒体氧化应激显著抑制鱼藤酮诱导的细胞凋亡。它减少小胶质细胞炎症并改善神经元存活。我们的结果表明,利福平在各种实验条件下具有细胞保护作用,并表明它可能对 PD 治疗有用。本文旨在综述使用利福平的实验性神经保护数据,重点介绍 PD 体外模型中细胞保护作用的分子和细胞机制。