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NRVMs (5000 cells/well) were plated in 24-well plates.
To evaluate heart ROS production in situ, frozen, unfixed, whole heart cross-sections or living NRVMs were stained with 10 [micro]mol/L DHE (Sigma) for 30 min in a dark humidified chamber at 37[degrees]C.
Cell viability assays were performed using doxorubicin-treated NRVMs. As shown in Figure 2(a), doxorubicin treatment reduced cell viability in a dose-dependent manner compared with the control; 0.1 [micro]M doxorubicin treatment led to 20% decreased cell viability.
As shown in Figure 3(a), NRVMs pretreated with 50 [micro]g/ mL APS attenuated doxorubicin-induced ROS generation.
We found that pretreatment with APS significantly attenuates doxorubicin-induced p38MAPK phosphorylation in a concentration-dependent manner in NRVMs (Figure 5(a)).
We also analyzed the time course of doxorubicin-induced Akt phosphorylation in NRVMs. As shown in Figure 5(d), doxorubicin dramatically increased Akt phosphorylation beginning with the 12 h treatment, and this was reduced at 48 h and further lowered at 72 h.
Accordingly, DNA laddering showed that the APS-mediated protection of doxorubicin-treated NRVMs could be abrogated by LY294002 (Figure 5(f)).
To explain the different phenomenon, we analyzed thetimecourseofdoxorubicin-induced Akt phosphorylation in NRVMs. Western blotting showed that phosphorylated Akt was elevated after doxorubicin treatment within a short period, which was reduced after 48 h.
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