Background and Objectives. Tourniquet-induced ischemia/reperfusion (I/R) injury is a common clinical problem for patients receiving surgery. The objective of this study is to determine if oxycodone (Oxy) reduces skeletal muscle I/R damage induced by tourniquet placement and explores the underlying mechanisms. Method. Mice were randomly assigned to the sham, I/R, Oxy, and I/R with Oxy groups. Oxy was injected intraperitoneally 30 min before tourniquet placement. Morphological changes of the gastrocnemius muscle in these mice were assessed by hematoxylin-eosin (HE) staining and electron microscopy. Expression levels of TLR4, NF-κB, SIRT1, and PGC-1α in the skeletal muscles were detected by western blot. Blood TNF-α levels, gastrocnemius muscle contractile force, and ATP concentration were examined. Results. Compared with the I/R group, Oxy pretreatment attenuated skeletal muscle damage, decreased serum TNF-α levels, and inhibited the expression levels of TLR4/NF-κB in the gastrocnemius muscle. Furthermore, Oxy treatment significantly increased serum ATP levels and the contractility of the skeletal muscles. SIRT1 and PGC-1α levels were significantly reduced in gastrocnemius muscle after I/R. Oxy pretreatment recovered these protein expression levels. Conclusion. Tourniquet-induced acute limb I/R results in morphological and functional impairment in skeletal muscle. Pretreatment with Oxy attenuates skeletal muscle from acute I/R injury through inhibition of TLR4/NF-κB-dependent inflammatory response and protects SIRT1/PGC-1α-dependent mitochondrial function.

中文翻译：

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激活阿片受体可减轻止血带放置引起的骨骼肌缺血/再灌注损伤

背景和目标。止血带引起的缺血/再灌注 (I/R) 损伤是接受手术的患者的常见临床问题。本研究的目的是确定羟考酮 (Oxy) 是否能减少因放置止血带而引起的骨骼肌 I/R 损伤，并探索其潜在机制。方法。小鼠被随机分配到假手术组、I/R、Oxy 和 I/R with Oxy 组。在放置止血带前 30 分钟腹膜内注射 Oxy。通过苏木精-伊红 (HE) 染色和电子显微镜评估这些小鼠腓肠肌的形态变化。通过蛋白质印迹检测骨骼肌中TLR4、NF-κB 、 SIRT1和PGC- 1α的表达水平。血液肿瘤坏死因子-α检查水平、腓肠肌收缩力和 ATP 浓度。结果。与 I/R 组相比，Oxy 预处理减轻了骨骼肌损伤，降低了血清 TNF -α水平，并抑制了腓肠肌中 TLR4/NF- κB的表达水平。此外，Oxy 治疗显着增加了血清 ATP 水平和骨骼肌的收缩力。I/R 后腓肠肌中SIRT1 和 PGC-1 α水平显着降低。氧预处理恢复了这些蛋白质表达水平。结论. 止血带引起的急性肢体 I/R 导致骨骼肌的形态和功能障碍。Oxy 预处理通过抑制 TLR4/NF- κB依赖性炎症反应减轻骨骼肌急性 I/R 损伤，并保护 SIRT1/PGC-1 α依赖性线粒体功能。