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Resisting cell death
Sustaining proliferative signaling
[Effects of postconditioning on autophagy of lung ischemic reperfusion injury in rats].
OBJECTIVE:
To explore the effects of postconditioning on autophagy of lung injury in situ during lung ischemic reperfusion.
METHODS:
Twenty-four male Sprague-Dawley rats were randomly divided into 3 groups of sham-operated (S), ischemic-reperfusion (I/R) and ischemic postconditioning (IpostC) (n = 8 each). All underwent left thoracotomy after anesthesia. In the S group, a line was only placed around left hilum but not fastened. In the I/R group, a line was fastened to block the blood flow of left lung for 30 min and then loosened for reperfusion for 120 min. In the IpostC group, after blocking the blood flow of left lung for 30 min, left hilum was fastened for 30 sec and loosened for 30 sec. Lung tissues were measured by Western blot. Histopathological changes of lung tissues were observed, lung injury scores calculated and autophagic vacuoles determined by electron microscope.
RESULTS:
The relative expression levels of mammalian target of rapamycin (mTOR) and phosphorylated mTOR (p-mTOR) in group I/R (0.40 +/- 0.03, 0.33 +/- 0.10) were not different with those of group S (0.37 +/- 0.07, 0.31 +/- 0.10) (both P > 0.05). However, both significantly increased in group IpostC (0.46 +/- 0.09, 0.55 +/- 0.07) (both P < 0.05). As compared with group S, the relative expression level of LC3-IIand lung injury score significantly increased in groups I/R and IpostC (0.53 +/- 0.08, 0.38 +/- 0.03 vs 0.25 +/- 0.06; 15.79 +/- 1.33, 11.67 +/- 1.55 vs 5.58 +/- 0.39) while obviously declined in group IpostC versus group I/R (all P < 0.05). In group I/R, neutrophil infiltration, interstitial edema, atelectasis and hyaline membrane formation were observed microscopically in lung tissues and the formation of autophagic vacuoles was evident under electron microscope. The changes of group IpostC were milder than those of group I/R.
CONCLUSIONS:
Ischemic postconditioning has protective effects on lung ischemic reperfusion injury by attenuating autophagy. It may be related with strengthening mTOR.
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