Fig. 9.

c1-treated cardiomyoblasts do not shut down Nrf2 activation as DOX does. Immunoblots for the transcriptional regulator Nrf2 (left) and one of its downstream targets, HO-1 (right), demonstrate stabilization of Nrf2 with concomitant expression of HO-1 in DMSO-treated samples; DOX treatment completely suppressed both, while c1 treatment was only moderately suppressive (n = 4 and n = 3 for Nrf2 and HO-1, respectively). The bar graphs below represent the mean ± SEM. Results were statistically different between c1 and DOX in both cases (p = 0.002 and p = 0.019), and more marginally so between c1 and DMSO (p = 0.011 and p. = 0.025), for Nrf2 and HO-1, respectively.