Cell membrane integrity and revascularization: The possible functional mechanism of ischemic preconditioning for skeletal muscle protection against ischemic-reperfusion injury

• Published in: Acta histochemica Vol. 119; no. 3; pp. 309 - 314
• Main Authors: Hong, Yang, Zhang, Bin, Yu, Ling, Duan, Shan-Shan
• Format: Journal Article
• Language: English
• Published: Germany Elsevier GmbH 01.04.2017
• Subjects: Animals; Cell Membrane - pathology; Cell Membrane - physiology; Fluorescent Antibody Technique; Ischemic Preconditioning; Ischemic-reperfusion injury; Male; Muscle, Skeletal - injuries; Muscle, Skeletal - physiology; Muscle, Skeletal - ultrastructure; Platelet Endothelial Cell Adhesion Molecule-1 - metabolism; Rats; Reperfusion Injury - prevention & control; Revascularization; Skeletal muscle; Ischemic preconditioning; Ischemic-reperfusion injury; Skeletal muscle; Revascularization
• ISSN: 0065-1281; 1618-0372
• DOI: 10.1016/j.acthis.2017.02.007

The purpose of this paper was to evaluate whether ischemic preconditioning (IPC) could make protective effects against skeletal muscle injuries induced by ischemic-reperfusion (I/R). Eighteen rats were randomly divided into three groups of 6 subjects each: control group, I/R group, and IPC group. Thigh root ischemia of rats in the I/R group was induced by 3h ischemia and 24h reperfusion. IPC was applied by 3 periods of 15min ischemia/15min reperfusion prior to ischemia. Morphological changes in skeletal muscle cells induced by I/R and IPC were observed by hematoxylin and eosin (HE) staining and electron microscopy. In addition, angiogenesis was evaluated by immunolabeling of CD31. IPC could prevented morphological alternations induced by ischemia, including myofilament, cell membrane, cell matrix, nucleus, mitochondria, and sarcoplasmic reticulum damage in skeletal muscle cells. The CD31 immunolabeling showed that neovascularization was observed in the IPC group but not in the I/R group. IPC could protect skeletal muscle cells from necrosis, apoptosis, and morphological damages induced by I/R injury. Revascularization may play a key role in the mechanism underlying the protective effects of IPC in vivo.