Microparticles Mediate Hepatic Ischemia-Reperfusion Injury and Are the Targets of Diannexin (ASP8597) (original) (raw)
Figure 3
MPs invoke mitochondrial permeability transition, oxidative stress, adhesion molecule expression and activate NF-κB in hepatocytes.
A. Hepatocytes loaded with 50 nM TMRM (red fluorescence), 1 µM DCFH2-DA (green fluorescence) and placed in chambers at 37°C for 15 min. MPT occurred with increasing MP concentrations, blocked by 1 µM CyA. B. 1 mM of NAC inhibited oxidative stress generated by MPs. C, D. Primary hepatocytes were exposed to 60 nM of MPs derived from liver 2 hr post-IR and pro-inflammatory molecules COX-2 and PKC-δ determined (WB) as well as (E) JNK-1/2 (46 kDA, 54 kDA) activation (phospho-JNK). * p<0.05 experimental groups vs. control. + p<0.05 30 and 60 nM vs. 12 nM MPs. † p<0.05 MPs 60 nM vs. 30 nM MPs. F. MPs activate NF-κB in primary hepatocytes, by IκB-α degradation (immunoblots). Blots represent three experiments conducted in triplicate (n = 9). * p<0.05 experimental vs. control.