Figure 7.

HNG reduces amyloid β-induced and mtDNA-mediated cell stress: Protective effects of pre-treatment with HNG against amyloid-β cytotoxicity were measured using the MTT assay. Amy-β Active (1-42) represents Amyloid-β_1–42 which is the active form; Amy-β SC(42-1) represents amyloid-β_42-1 which is the scrambled, inactive form that serves as control. (a) Compared to untreated (UN)-normal (NL) cybrids, Amy-β Active (1-42)-treated NL cybrids showed a 35% (P<0.001, n=4) reduction in cell viability. No differences in cell viability were observed between untreated-NL cybrids and Amy-β SC(42-1)-treated NL or HNG-treated NL. Cell viability was significantly higher (31.25%, P<0.05, n=4) for Amy-β SC(42-1)-treated NL cybrids versus Amy-β Active (1-42)-treated NL cybrids. HNG increased cell viability by 35.94% (P<0.05, n=4) in Amy-β Active (1-42)-treated NL cybrids compared to the NL cybrids treated with Amy-β Active (1-42)-treated alone (Supplementary Table S10A). (b) Treatment of AMD cybrids with Amy-β Active (1-42) alone reduced cell viability by 41.8% (P<0.05, n=3–4) compared to untreated-AMD cybrids. No difference in cell viability was observed between untreated-AMD cybrids and Amy-β SC(42-1)-treated AMD cybrids. Significant reduction in cell viability was observed in Amy-β Active (1-42)-treated AMD cybrids (94.9%, P<0.01, n=3–4) compared to the Amy-β SC(42-1)-treated AMD cybrids. AMD cybrids treated with HNG alone had a 42.4% increase in cell viability compared to untreated-AMD cybrids (P<0.05, n=3–4). Pre-treatment with HNG increased cell viability by 107.7% in Amy-β Active (1-42)-treated AMD cybrids (P<0.001, n=3–4) compared to the AMD cybrids treated with active Amy-β Active (1-42) alone (Supplementary Table S10B). Data are represented as mean±S.E.M., normalized to untreated-normal cybrids (assigned value of 1). The endpoint for all experiments was 72 h