Neuroinflammation and oxidative stress cooperate to compromise the function of the central nervous system (CNS). Colloidal platinum nanoparticles (Pt NPs) are ideal candidates for reducing the deleterious effects of neuroinflammation since they act as free radical scavengers. Here we evaluated the effects of Pt NPs on several markers of lipopolysaccharide (LPS)-induced inflammation in cultured BV-2 microglial cells. BV-2 cells were treated with increased dilutions (1–100 ppm) of Colloidal Pt and/or LPS (1–10 µg/mL) at different exposure times. Three different protocols of exposure were used combining Pt NPs and LPS: (a) conditioning-protective effect (pre–post-treat), (b) therapeutic effect (co-treat) and (c) conditioning-therapeutic effect (pre-co-treat). After exposure to LPS for 24 h, cells were used for assessment of cell viability, reactive oxygen species (ROS) generation, lactate dehydrogenase (LDH) activity, apoptosis and caspase-3 levels, cell proliferation, mitochondrial membrane potential, inducible nitric oxide (iNOS) activity, pro-inflammatory cytokine (IL-1β, TNF-α and IL-6) levels, and phagocytic activity. Low concentrations (below or equal to 10 ppm) of Colloidal Pt prevented or ameliorated the LPS-induced increase in ROS formation, loss of mitochondrial membrane potential, induction of apoptosis, increase in LDH release, increase in pro-inflammatory cytokines and iNOS, inhibition of phagocytosis linked to microglial persistence in the M1 phase phenotype, loss of cell adhesion, differentiation and/or proliferation, as well as loss of cell viability. These protective effects were evident when cells were preconditioned with Pt NPs prior to LPS treatment. Collectively, the findings demonstrate that at low concentrations, Pt NPs can regulate the function and phenotype of BV-2 cells, activating protective mechanisms to maintain the microglial homeostasis and reduce inflammatory events triggered by the inflammatory insults induced by LPS. These preventive/protective effects on the LPS pro-inflammatory model are linked to the antioxidant properties and phagocytic activity of these NPs.

神经炎症和氧化应激共同损害中枢神经系统（CNS）的功能。胶体铂纳米粒子（Pt NP）是减少神经炎症有害影响的理想候选者，因为它们充当自由基清除剂。在这里，我们评估了 Pt NP 对培养的 BV-2 小胶质细胞中脂多糖 (LPS) 诱导的炎症的几种标志物的影响。在不同的暴露时间下，用增加稀释度 (1–100 ppm) 的胶体 Pt 和/或 LPS (1–10 µg/mL) 处理 BV-2 细胞。结合 Pt NP 和 LPS 使用三种不同的暴露方案：（a）调理-保护作用（治疗前），（b）治疗效果（共同治疗）和（c）调理-治疗效果（治疗前） -对待）。暴露于LPS 24小时后，细胞用于评估细胞活力，活性氧 (ROS) 生成、乳酸脱氢酶 (LDH) 活性、细胞凋亡和 caspase-3 水平、细胞增殖、线粒体膜电位、诱导型一氧化氮 (iNOS) 活性、促炎细胞因子（IL-1β、TNF-α 和IL-6）水平和吞噬细胞活性。低浓度（低于或等于 10 ppm）的胶体 Pt 可预防或改善 LPS 诱导的 ROS 形成增加、线粒体膜电位丧失、诱导细胞凋亡、LD​​H 释放增加、促炎细胞因子和 iNOS 增加、抑制吞噬作用的降低与小胶质细胞在 M1 期表型的持续存在、细胞粘附、分化和/或增殖的丧失以及细胞活力的丧失有关。当在 LPS 处理之前用 Pt NP 预处理细胞时，这些保护作用是明显的。总的来说，研究结果表明，在低浓度下，Pt NP 可以调节 BV-2 细胞的功能和表型，激活保护机制以维持小胶质细胞稳态，并减少由 LPS 诱导的炎症损伤引发的炎症事件。这些对 LPS 促炎模型的预防/保护作用与这些 NP 的抗氧化特性和吞噬活性有关。