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细胞膜完整性与血管再生:缺血预处理对骨骼肌保护以抵御缺血再灌注损伤的可能功能机制。

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

作者信息

Hong Yang, Zhang Bin, Yu Ling, Duan Shan-Shan

机构信息

Department of Orthopedics, Shanghai No.5 Hospital, Fudan University, Shanghai 200240, China.

Department of Orthopedics, Shanghai Wujing Hospital, Shanghai 200240, China.

出版信息

Acta Histochem. 2017 Apr;119(3):309-314. doi: 10.1016/j.acthis.2017.02.007. Epub 2017 Mar 11.

DOI:10.1016/j.acthis.2017.02.007
PMID:28291543
Abstract

BACKGROUND

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).

METHODS

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.

RESULTS

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.

CONCLUSION

Revascularization may play a key role in the mechanism underlying the protective effects of IPC in vivo.

摘要

背景

本文旨在评估缺血预处理(IPC)是否能对缺血再灌注(I/R)诱导的骨骼肌损伤产生保护作用。

方法

将18只大鼠随机分为3组,每组6只:对照组、I/R组和IPC组。I/R组大鼠通过3小时缺血和24小时再灌注诱导大腿根部缺血。在缺血前通过3个周期的15分钟缺血/15分钟再灌注进行IPC。通过苏木精和伊红(HE)染色及电子显微镜观察I/R和IPC诱导的骨骼肌细胞形态学变化。此外,通过CD31免疫标记评估血管生成。

结果

IPC可预防缺血诱导的形态学改变,包括骨骼肌细胞中的肌丝、细胞膜、细胞基质、细胞核、线粒体和肌浆网损伤。CD31免疫标记显示,IPC组观察到新生血管形成,而I/R组未观察到。IPC可保护骨骼肌细胞免受I/R损伤诱导的坏死、凋亡和形态学损伤。

结论

血管再生可能在IPC体内保护作用的潜在机制中起关键作用。

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