Mulberrin Confers Protection against Doxorubicin-Induced Cardiotoxicity via Regulating AKT Signaling Pathways in Mice

Figure 6

AKT inhibition abolished the anti-inflammatory and antioxidative activities of mulberrin in DOX-stimulated cells. The phosphorylation of AKT, GSK3β, and mTOR (a) was detected in the indicated groups. Cell viability was detected in cells treated with an AKT inhibitor (b). Cardiomyocyte injury was assayed by the release of LDH (c). The ROS level (d) and MDA content (e) were detect to reflect oxidative damage caused by DOX in cells incubated with an AKT inhibitor. Luciferase assay (f) was used to reflect NF-κB transactivation in vitro. The mRNA level of TNF-α (g) in cells incubated with an AKT inhibitor. Data are presented as . for each group. For (a), compared with the saline group; ^# compared with DOX alone. For others, compared with the control groups.

(a)

(b)

(c)

(d)

(e)

(f)

(g)