Fig. 2: Response of BV2 microglial cells and astrocytes to soluble Abeta42 (Aβ) aggregates (oligomers) and the blocking of the TNF-α production by TLR4 antagonists. | Communications Biology

Fig. 2: Response of BV2 microglial cells and astrocytes to soluble Abeta42 (Aβ) aggregates (oligomers) and the blocking of the TNF-α production by TLR4 antagonists.

From: Beta amyloid aggregates induce sensitised TLR4 signalling causing long-term potentiation deficit and rat neuronal cell death

Fig. 2

a Time course of TNF-α production by BV2 cells in response to continual exposure to soluble Aβ oligomers (10 pM–1 nM) together with monomer (monomer concentration 0.002–0.2 μM) (n = 4, sem). b The response of astrocytes to Aβ monomers, Aβ oligomers together with monomer (oligomer concentration 0.25 to 1000 nM and total monomer concentration 0.05–200 μM) and Aβ fibrils (total monomer concentration) compared to LPS (0.05–200 ng/ml) stimulation for 24 h (n = 4, mean ± sem). The astrocyte preparation had <2% microglial. c Time course of TNF-α production by astrocyte cells in response to continual exposure to Aβ oligomers (10 pM–1 nM) together with monomer (total monomer concentration 0.002–0.2 μM) (n = 4, mean ± sem). d The response of astrocytes after a 24 h incubation with Aβ oligomers (0.05–200 nM oligomer) together with monomer (total monomer 0.01–40 μM)) only and together with the TLR4 antagonist RSLA (0.1 µg/ml), LPS and RSLA, RSLA only and the TLR4 antagonist TAK-242 (1 µM) alone and with Aβ oligomers and monomer (n = 4, mean ± sem).

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