1. Hyperbaric oxygen preconditioning inhibits skin flap apoptosis in a rat ischemia-reperfusion model.
- Author
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Xiao YD, Liu YQ, Li JL, Ma XM, Wang YB, Liu YF, Zhang MZ, Zhao PX, Xie F, and Deng ZX
- Subjects
- Animals, Caspase 3 metabolism, Disease Models, Animal, MAP Kinase Kinase Kinase 5 metabolism, Male, Proto-Oncogene Proteins c-bcl-2 metabolism, Random Allocation, Rats, Sprague-Dawley, Reperfusion Injury metabolism, Reperfusion Injury pathology, Skin metabolism, Skin pathology, bcl-2-Associated X Protein metabolism, Apoptosis, Hyperbaric Oxygenation, Ischemic Preconditioning methods, Reperfusion Injury prevention & control, Skin blood supply
- Abstract
Background: Hyperbaric oxygen (HBO) improves skin flap function and inhibits partial necrosis induced by ischemia-reperfusion (I/R) injury. Our study aimed to evaluate the mechanism underlying HBO regulation of the antiapoptosis factors associated with I/R injury of skin flaps., Methods: The rats were divided into sham surgery, I/R, and HBO groups. Rats from the HBO group received HBO preconditioning followed by I/R surgery. Blood perfusion of the skin flaps was measured with laser Doppler flowmeters. Tissue morphology and apoptosis were subsequently assessed based on hematoxylin-eosinhe and terminal deoxynucleotidyl transferase dUTP nick-end labeling staining. Protein expression of phosphorylated apoptosis signal-regulating kinase 1 (pASK-1), phosphorylated c-Jun N-terminal kinase (pJNK), B-cell lymphoma-2 (Bcl-2), and Bcl2-associated X protein (Bax) was examined by immunodetection, and Bcl-2 messenger RNA expression was detected by quantitative polymerase chain reaction. In addition, caspase-3 activity was also measured., Results: The result of microcirculation analysis showed that the survival and blood perfusion rates significantly increased in the skin flap after HBO exposure. Terminal deoxynucleotidyl transferase dUTP nick-end labeling staining revealed that cell apoptosis was significantly attenuated in the HBO group. Furthermore, HBO preconditioning increased the expression of Bcl-2 and inhibited pASK-1, pJNK, and Bax expression as determined by both immunohistochemistry and Western blot. Caspase-3 activity and the Bax/Bcl-2 ratio declined in the HBO group., Conclusions: HBO preconditioning effectively ameliorates I/R injury by regulating the apoptosis signal-regulating kinase 1 and/or c-Jun N-terminal kinase pathway and anti- and proapoptosis factors., (Copyright © 2015 Elsevier Inc. All rights reserved.)
- Published
- 2015
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