Fig. 9. Role of Nrf2 and NF-κB signals in CAR-offered protection against LPS-induced cardiomyocyte contractile dysfunction.

Mouse cardiomyocytes from adult C57BL/6 mice were exposed to LPS (4 μg/mL) for 6 h in the absence or presence of CAR (10 µM), the Nrf2 inhibitor ML-385 (20 μM), or the NF-κB activator prostratin (2 μM). a resting cell length; b peak shortening (PS); c maximal velocity of shortening (+dL/dt); d maximal velocity of relengthening (−dL/dt); e time-to-peak shortening (TPS); and f time-to-90% relengthening (TR₉₀). Mean ± SEM, n = 30 cells from three mice per group, *P < 0.05 vs the control group, ^#P < 0.05 vs the LPS group, ^†P < 0.05 vs the LPS-CAR group.