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. 2014 Aug 4;142(1):6–20. doi: 10.1093/toxsci/kfu158

FIG. 8.

FIG. 8.

Effect of compound C, rapamycin, bafilomycin A1, and 3-MA on paraquat-induced cardiomyocyte contractile defects. Freshly isolated cardiomyocytes from WT mice were incubated with paraquat (100 μM) in the presence or absence of the AMPK inhibitor compound C (5 μM), rapamycin (5 μM), lysosomal inhibitor bafilomycin A1 (100 nM), and 3-MA (10 mM) for 3 h. (A) Resting cell length; (B) peak shortening (normalized to resting cell length); (C) maximal velocity of shortening (+ dL/dt); (D) maximal velocity of relengthening (− dL/dt); (E) time-to-peak shortening (TPS); (F) time-to-90% relengthening (TR90). Mean ± SEM, n = 64–157 cells from four mice per group; *p < 0.05 versus control group, #p < 0.05 versus paraquat group, p < 0.05 versus paraquat compound C group.