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. 2011 Nov 1;15(9):2407–2424. doi: 10.1089/ars.2010.3751

FIG. 10.

FIG. 10.

Effect of the mPTP inhibitor cyclosporine A, the GSK3β inhibitor SB216763 and the ER stress inhibitor TUDCA on TN-induced cardiomyocyte contractile dysfunction. Freshly isolated murine cardiomyocytes were incubated with TN (3 μg/ml) for 5–6 h in vitro in the absence or presence of cyclosporine A (200 nM), SB216763 (10 μM), or TUDCA (500 μM) before assessment of mechanical properties. (A) Resting cell length; (B) PS (% of resting cell length); (C) maximal velocity of shortening (+dL/dt); (D) maximal velocity of relengthening (−dL/dt); (E) TPS; and (F) time-to-90% relengthening (TR90). Mean±SEM, n=52–53 cells per group, *p<0.05 versus control (without drug treatment) group; #p<0.05 versus TN group.