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. 2020 Nov 1;11(3):680–693. doi: 10.1016/j.apsb.2020.10.017

Figure 6.

Figure 6

YAP1 was involved in the protection of isorhapontigenin (Isor) on Dox-induced cardiotoxic effects. NRCMs were transfected with sgRNA targeting Yap1 or treated with YAP1 inhibitor Dob (10 μmol/L) before Dox (1 μmol/L) and Isor (10 μmol/L) co-treatment. Cell viability was measured by CCK-8 (A). The cell morphology was observed by light microscopy, and scale bar was 200 μm (B) and (F). The nuclear condensation and TUNEL positive staining cells were observed and scale bar was 400 μm (C) and (G). The protein change of cleaved caspase 3 was measured by Western blot (D) and (H). The mitochondrial membrane potential changes of NRCMs were detected by TMRE staining, and scale bar was 400 μm (E) and (I). Data were expressed as mean ± SEM, n = 6; ∗∗P < 0.01 vs. control group; #P < 0.05, ##P < 0.01 vs. Dox group; $P < 0.05, $$P < 0.01 vs. Dox+Isor group. Isor, isorhapontigenin; Dox, doxorubicin; NRCMs, neonatal rat cardiomyocytes; Dob, dobutamine; TMRE, tetramethylrhodamine ethyl ester perchlorate; YAP1, Yes-associated protein 1.