Fig. 1.
Effect of TQ and Aβ1–42 on cell viability and apoptosis in hiPSC-derived cholinergic neurons. (A) The group treated with Aβ1–42 (5 μM) had a significant 36.5% loss in their viability. In the group treated with Aβ1–42 and TQ (100 nM), TQ prevented Aβ1–42 induced cell death by restoring the cell viability to 90%. Cultures were treated for 48 h and viability was assessed with Cell Titer – Glo assay. (*P < 0.05 vs. control) n = 4. (B) Aβ1–42 (5 μM) treated group had a significant 90% increase in caspase 3/7 activities comparing to controls. However, simultaneous treatment with TQ (100 nM) abolished the activities to control levels significantly. Cultures were treated for 48 h and activities of caspase 3 and 7 were measured with Caspase-Glo 3/7 assay. (**P < 0.01: the group exposed to Aβ1–42 alone vs. control, vs. TQ+ Aβ1–42 group, vs. TQ alone), n = 5. Values shown are the mean percent luminescence (where 100% = luminescence in control hiPSC-derived cholinergic neurons), ± Standard Error of the Mean (SEM). Data were analyzed by one-way ANOVA, followed by the Holm-Bonferroni method.