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. Author manuscript; available in PMC: 2015 Apr 28.
Published in final edited form as: J Alzheimers Dis. 2015 Jan 1;45(3):933–946. doi: 10.3233/JAD-142217

Figure 1. CAW induces anti-oxidant response in MC65 and SH-SY5Y cells.

Figure 1

A) Aβ accumulation, in MC65 cells grown without tetracycline (Tet−), significantly increased intracellular ROS levels at both 24h and 48h. CAW treatment (100ug/mL) attenuated that increase (n=12–16 per treatment condition). B) Treatment with Aβ25–35 peptide (50uM) induced intracellular ROS in SH-SY5Y cells at 24h and 48h. CAW (100ug/mL) significantly reduced that increase (n=12–16 per treatment condition). C) At 24h, CAW treatment following tetracycline withdrawal significantly induced the expression of a panel of antioxidant response genes in MC65 cells. After 48h induction was even greater in the Tet− condition as well as cells treated with CAW in the absence of tetracycline. CAW treatment in the presence of tetracycline also significantly induced antioxidant gene expression but only at the 48h time point. (n=6–7 per treatment condition) D) In SH-SY5Y cells Aβ treatment significantly induced the expression of NFE2L2 and its target genes at both 24h and 48h. CAW treatment potentiated this increase at both time points. CAW treatment also significantly induced expression of the antioxidant response genes at both time points but to a lesser extent than CAW and Aβ together (n=6 per treatment condition). *p<0.05, **p<0.01, ***p<0.001 relative to either Tet+ or Control unless otherwise indicated.