Research Paper Volume 10, Issue 8 pp 2122—2135
A Drosophila model of cigarette smoke induced COPD identifies Nrf2 signaling as an expedient target for intervention
Figure 6. Oltipraz ectopically activates Nrf2 signaling and increases lifespan of CS exposed flies. CS exposure impacts the expression of GFP in Nrf2 reporter lines (A-D). 3rd instar ARE-GFP larvae were left untreated (A) or exposed to CS (B). GstD2-GFP animals left untreated (C) or CS exposed (D). Impact of oltipraz on the activation of Nrf2 signaling in 3rd instar larvae (E-H). 3rd instar ARE-GFP larvae were left untreated (E) or exposed to oltipraz (F). GstD2-GFP animals left untreated (G) or treated with oltipraz (H). Effect of oltipraz on the transcript levels of canonical Nrf2 target genes (J, N=3, means ±S.D., n = 5, p > 0.01 for gstd5). Lifespan analysis of CS exposed animals (daily doses) that were left otherwise untreated (red symbols) or that were chronically confronted with oltipraz (blue symbols) (p<0.001, n = 5).