Figure 1
SCM-198 inhibited lipopolysaccharide (LPS)- or Aβ 1-40 -induced proinflammatory mediator release in microglia and astrocytes. BV-2 cells were pretreated with indicated concentrations of SCM-198(SCM) or ibuprofen (IBU) for 2 hours, then stimulated with 1 μg/ml LPS for another 2 hours. mRNA expressions of iNOS (a), TNF-α (b), IL-1β (c) and IL-6 (d) were analyzed by real-time RT-PCR. BV-2 cells were pretreated with indicated concentrations of SCM or IBU for 2 hours, followed by 24-hour incubation with 1 μg/ml LPS, nitric oxide (NO) (e), IL-1β (f), TNF-α (g) levels in the cell culture medium were detected by Griess reaction and ELISA assay, respectively. Primary microglia were pretreated the same way as described above, followed by 24-hour incubation with 1 μg/ml LPS. TNF-α (h) level in the cell culture medium was measured by ELISA assay. BV-2 cells were pretreated with the indicated concentrations of SCM or 20 μM donepezil (DON) for 2 hours, followed by 24-hour stimulation with 3 μM Aβ1-40. TNF-α (i) in the cell culture medium was measured by ELISA assay. Primary astrocytes were pretreated with indicated concentrations of SCM or 20 μM donepezil (DON) for 2 hours, followed by 48-hour stimulation with 10 μM Aβ1-40. NO (j) and TNF-α (k) levels in the cell culture medium was measured by Griess reaction and ELISA assay, respectively. *P < 0.05, **P < 0.01, ***P < 0.001, Tukey’s test versus only LPS- or only Aβ1-40-treated group; #P < 0.05, ##P < 0.01, ###P < 0.001, Tukey’s test versus control group.