Zhang Aihui, Wu Laiwei, Chen Zilin, Huang Guoqiang, Lu Xiaohe
1 Department of Ophthalmology, Liaocheng Brain Hospital affiliated to Liaocheng People's Hospital, Liaocheng, People's Republic of China.
2 Southern Medical University, Guangzhou, People's Republic of China.
Int J Toxicol. 2017 Sep/Oct;36(5):403-409. doi: 10.1177/1091581817718473. Epub 2017 Jul 21.
Classically activated macrophages (M1) are proinflammatory effectors and closely related to the progression of neurotoxicity. As a powerful psychostimulant and addictive drug, methamphetamine (Meth) abuse could result in long-lasting abnormalities in retina. This study investigated the effect of Meth at nontoxic concentration on macrophage activation state and its resultant toxicity to photoreceptor cells. Results showed that cytotoxicity was caused by Meth on 661 W cells after coculturing with RAW264.7 macrophage. RAW264.7 cells tended to switch to the M1 phenotype, releasing more proinflammatory cytokines after treatment with Meth. Meth could also upregulate the M1-related gene and protein expression. Our study demonstrated that Meth promoted macrophage polarization from M0 to M1 and induced inflammatory response, providing the scientific rationale for the photoreceptor cell damage caused by the Meth abuse.
经典活化的巨噬细胞(M1)是促炎效应细胞,与神经毒性的进展密切相关。作为一种强大的精神兴奋剂和成瘾性药物,甲基苯丙胺(冰毒)滥用可导致视网膜长期异常。本研究调查了无毒浓度的冰毒对巨噬细胞活化状态的影响及其对光感受器细胞的毒性。结果表明,与RAW264.7巨噬细胞共培养后,冰毒对661W细胞产生了细胞毒性。RAW264.7细胞在经冰毒处理后倾向于转变为M1表型,释放更多促炎细胞因子。冰毒还可上调M1相关基因和蛋白表达。我们的研究表明,冰毒促进巨噬细胞从M0极化到M1并诱导炎症反应,为冰毒滥用导致的光感受器细胞损伤提供了科学依据。