Research Paper Volume 13, Issue 18 pp 22556—22570

MSCs enhances the protective effects of valsartan on attenuating the doxorubicin-induced myocardial injury via AngII/NOX/ROS/MAPK signaling pathway


Figure 1. The cell viability determination and effect of Val pre-treatment followed by DOX-exposure on ROS level and apoptosis rate in H9c2 cells. (A) Effect of DOX on H9c2 cells viability for 24 h. (B) Effect of Val on H9c2 cells viability for 24 h. (C) Effect of Val at three concentrations on H9c2 cells over time. (D) Viability of DOX-induced H9c2 cells followed as three of Val concentrations pre-treatment. (E, F) Effect of Val and DOX on tumor cells viability. (G) Effect of Val pre-treatment on the ROS level of DOX-treated H9c2 cells at different time points. (H) Effect of Val on apoptosis of DOX-treated H9c2 cells. (I) Microscopic analysis of Val and DOX-treatment on ROS levels by DCF Fluorescence. (J) The bar graph of the quantitative analysis of apoptosis rate of H9c2 cells. *P<0.05 vs. Control; †P<0.05 vs. DOX. DOX, doxorubicin; Val, valsartan.