Fig. 3

Ionomycin A or thapsigargin induced excessive production of proinflammatory cytokines IL-1β and TNF-α in comparison with treatment with Aβ1-42. a, b THP-1 cells were incubated with either the vehicle only (−), ionomycin A (4 μM), thapsigargin (2 μM), or Aβ1-42 (10 μM) for 16 h. c, d THP-1 cells were pretreated with EGTA (0.5 mM) for 30 min followed by incubation with either the vehicle only (−) or Aβ1-42 (10 μM) for 16 h. Levels of IL-1β (a, c) or TNF-α (b, d) in supernatants were quantitated by ELISA. Ionomycin A and thapsigargin mimicked Aβ1-42-mediated effects, increasing the production and release of IL-1β and TNF-α whereas depletion of Ca²⁺ with EGTA attenuated Aβ1-42-evoked responses. Values are expressed as means ± SEM of at least six independent experiments measured in duplicates. **P < 0.01, versus vehicle-treated samples; ^##P < 0.01, compared to Aβ1-42-treated samples. Aβ, amyloid-β; EGTA, ethylene glycol trtraacetic acid; IL-1β, interleukin 1-β; TNF-α, tumor necrosis factor-α