PGC-1α Protects against Hepatic Ischemia Reperfusion Injury by Activating PPARα and PPARγ and Regulating ROS Production

Figure 7

Inhibition of either PPARα or PPARγ alleviates the effect of PGC-1α on ROS production induced by liver I/R injury, and NAC pretreatment significantly reduces the aggravating effects of PGC-1α knockdown on A/R-induced hepatocyte injury. (a) The representative images of DHE-stained liver cryosections from mice subjected to Ad-PGC-1α, Ad-PGC-1α+MK886, Ad-PGC-1α+GW9662, and Ad-PGC-1α+MK886+GW9662, relative to the Ad-GFP control at 1 h after I/R, and the relative ROS levels. Bar: 200 μm (). (b) The representative photographs of the DHE-stained hepatocytes subjected to Ad-PGC-1α, Ad-PGC-1α+MK886, Ad-PGC-1α+GW9662, and Ad-PGC-1α+MK886+GW9662, relative to the Ad-GFP control at 1 h after A/R, and the relative ROS levels in the hepatocytes of each group; bar: 200 μm (). (c) The Ad-shScramble- and Ad-shPGC-1α-transduced hepatocytes were pretreated with NAC for 1 h before the onset of A/R, respectively. At 24 h after A/R, the cell viability was determined by a CCK-8 assay (). (d) DNA fragmentation was determined at 24 h after A/R by the Cell Death Detection ELISA assay (). (e) LDH release was measured in each group (). (f) The DHE staining of the Ad-shScramble- and Ad-shPGC-1α-transduced hepatocytes at 1 h after A/R, with or without NAC pretreatment, and the relative ROS levels. Bar: 200 μm (). , , and .

(a)

(b)

(c)

(d)

(e)

(f)