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. 2019 Jun 2;2019:6173685. doi: 10.1155/2019/6173685

Figure 6.

Figure 6

ZYZ-803 downregulates RIP3-CaMKII signaling in ERS injury. (a) Data of RIP3 expression in cardiomyocytes treated by RIP3-siRNA/NS-siRNA. (b) LDH release of RIP3 knockdown and WT cardiomyocytes pretreated by ZYZ-803 (10 μM) for 1 h before tunicamycin injury. (c) Protein expression of RIP3 in cardiomyocytes (n = 3 independent experiments). (d, e) Analytical data of p-/t-CaMKII expression in cardiomyocytes (n = 3 independent experiments). (f) Coimmunoprecipitation of RIP3 and CaMKII was blocked by ZYZ-803 preconditioning in heart tissues (n = 3 independent experiments). Data are defined as mean ± SEM, one-way ANOVA. Compared with the Tuni group (NS-siRNA), # P < 0.001, ## P < 0.001; compared to the Tuni group (RIP3-siRNA), ∗ P < 0.05, ∗∗ P < 0.01, and ∗∗∗ P < 0.001; Tuni (NS-siRNA) versus the Tuni group (RIP3-siRNA), $ P < 0.01, $$ P < 0.05. (g) Immunofluorescent colocalization was decreased by ZYZ-803 in cardiomyocytes; scale bar (yellow): 50 μm.