Reversal of β-Amyloid-Induced Microglial Toxicity In Vitro by Activation of Fpr2/3

Figure 3

Neither treatment with oAβ nor QC1 affected major cellular antioxidant systems. (a) The ratio of reduced (GSH) to oxidised (GSSG) glutathione within BV2 cell cytoplasm was not affected by either oAβ (100 nM, 2 hrs) or QC1 (100 nM, 10 min post-oAβ) administration. (b) Expression of the antioxidant enzyme haem oxygenase-1 (HO-1) was not affected by treatment with oAβ (100 nM, 6 hrs) or QC1 (100 nM, 10 min post-oAβ). Sample loading was normalised to Ponceau S-defined total protein content; densitometric analysis data are of 3 independent cultures. (c) Expression of the antioxidant enzyme superoxide dismutase 2 (SOD2) was not affected by treatment with oAβ (100 nM, 24 hrs) or QC1 (100 nM, 10 min post-oAβ) or the alternative Fpr2/3 agonist Cpd43 (100 nM, 10 min post-oAβ). All western blot analyses are representative of 3 independent cultures, with sample loading normalised to Ponceau S-defined total protein content; densitometric analysis data are of 3 independent cultures, quantified in triplicate.

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