Fig. 1

PM2.5 exposure aggravates oAβ-induced neuronal injury and inflammation in neurons-microglia co-cultures via increasing IL-1β production. In transwell co-culture system, neurons in the neuronal medium were plated in the lower chamber. Before co-culture, microglia were activated with LPS (1 μg/ml) for 3 h (LPS priming). Inserts containing microglia were washed with fresh serum-free DMEM and then plated in the upper chamber. Then, neurons-microglia co-cultures were treated with or without oAβ (5 μM). After 12 h, neurons-microglia co-cultures were treated with or without PM2.5 (50 μg/ml) for 4 h. a, b Apoptosis of co-cultured neurons was evaluated by flow cytometry with annexin V/PI staining. c Cell viability of co-cultured neurons was assessed via MTT assay. *P < 0.05 vs. neurons in co-cultures with LPS-primed microglia. ^#P < 0.05 vs. neurons in co-cultures with oAβ-stimulated microglia. ^†P < 0.05 vs. neurons in co-cultures with PM2.5-oAβ-stimulated microglia. d Microglia were activated with LPS (1 μg/ml) for 3 h (LPS priming), and then oAβ (5 μM) was added into the culture medium. After 12 h, the cells were stimulated with PM2.5 (50 μg/ml) for 4 h. The concentration of IL-1β in the culture supernatant was then measured by ELISA. e The cells were stimulated with PM2.5 (0, 50, 100, 200 μg/ml) for 4 h. The concentration of IL-1β in the culture supernatant was measured by ELISA. All figures are representative of three independent experiments, performed in triplicate. *P < 0.05 vs. LPS-primed microglia. ^#P < 0.05 vs. LPS-primed microglia stimulated with oAβ