Figure 5
CaMKII positively regulated DOX-induced cardiomyocyte apoptosis by activating NF-κB. (a) Representative immunoblots of CaMKII, phosphorylated CaMKII, NF-κB, phosphorylated NF-κB, cleaved caspase 3, and GAPDH in NRVMs treated with or without AIP (10 μM, 24 h) in the presence or absence of DOX (10 μM) for 24 hours (n = 5–6). (b–d) Quantitative analysis of phosphorylated CaMKII, phosphorylated NF-κB, and cleaved caspase 3 in each group (n = 5–6). The experiment was conducted 3 times. (e) Apoptosis evaluated by TUNEL staining in each group (n = 5). The experiment was conducted 2 times. (f) Representative immunoblots of NF-κB, phosphorylated NF-κB, cleaved caspase 3, and GAPDH in NRVMs treated with or without PDTC (100 μM, 24 h) in the presence or absence of DOX (10 μM) for 24 hours (n = 5–6). (g–i) Quantitative analysis of phosphorylated NF-κB and cleaved caspase 3 in NRVMs treated with or without PDTC (100 μM, 24 h) in the presence or absence of DOX (10 μM) for 24 hours (n = 5–6). The experiment was conducted 2 times. (j) Apoptosis evaluated by TUNEL staining in each group (n = 5). The experiment was conducted 2 times. *P < 0.05, **P < 0.01: post-hoc Tukey’s comparison test.
