Remote Ischemic Preconditioning Protects against Liver Ischemia-Reperfusion Injury via Heme Oxygenase-1-Induced Autophagy
Figure 1
Hepatic inflow occlusion and reflow increased hepatic HO-1 and autophagic signaling.
(A) Western blotting for HO-1 and LC3-II in liver lysates from sham-operated or IR-treated mice shows increased HO-1 and LC3-II in the IR group, and the expression of HO-1, LC3-II peaked at 6–12 h and 12–24 h, respectively(*P<0.05 compared with the sham group). (B) Transmission electron microscopy of a 12-h liver sample after reperfusion revealed increased autophagosome formation (black arrows). (C) The data were quantified by counting the number of autophagosomes per cross-sectioned cell (*P<0.05 compared with sham group, n = 15). (D) The intensity of immunostaining of LC3-II (yellow) significantly increased after IRI compared with the sham group (*P<0.05 compared with the sham group). (E) The optical density of LC3-II immunostaining in the 12-h IR group was higher than in the sham group (*P<0.05 compared with the sham group).