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Fig. 2 | Journal of Neuroinflammation

Fig. 2

From: Sulforaphane rescues amyloid-β peptide-mediated decrease in MerTK expression through its anti-inflammatory effect in human THP-1 macrophages

Fig. 2

Aβ1-42-mediated reduction of MerTK expression is associated with increased intracellular Ca2+ level compared to treatment with ionomycin A or thapsigargin. a Intracellular Ca2+ images were obtained by Fluo-3AM method at 8 h after treatment with either the vehicle only (−), ionomycin A (4 μM), thapsigargin (2 μM), or 10 μM Aβ1-42 in THP-1 macrophages. b Histogram showing the ratio of intracellular Ca2+ levels to vehicle-treated group. c THP-1 cells were incubated with either the vehicle only (−), ionomycin A (4 μM), thapsigargin (2 μM), or Aβ1-42 (10 μM) for 8 h. d Densitometric quantification of analyses of c showing levels of MerTK protein. e 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 8 h. Total cell lysates were examined for MerTK via immunoblot. MerTK expression was decreased when intracellular Ca2+ levels were increased by ionomycin A, thapsigargin, or Aβ1-42. In contrast, the Aβ1-42-mediated decrease of MerTK protein was attenuated by depletion of Ca2+ with EGTA. Results are representative of three independent experiments. f Densitometric quantification of analyses of e showing levels of MerTK protein. All data are presented as means ± SEM (n = 3). **P < 0.01, versus vehicle-treated samples; ##P < 0.01, compared to Aβ1-42-treated samples. Aβ, amyloid-β; EGTA, ethylene glycol trtraacetic acid; MerTK, Mer tyrosine kinase

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