未经证实：止血带诱导的缺血和再灌注（I/R）通过涉及蛋白质合成/分解的机制与术后肌肉萎缩有关，细胞代谢，线粒体功能障碍，和凋亡。缺血预处理（IPC）可以保护骨骼肌免受I/R损伤。这项研究旨在确定IPC的潜在机制及其对全膝关节置换术（TKA）后肌肉力量的影响。
未经证实：24名TKA患者随机接受假IPC或IPC（3个周期的5分钟缺血，然后5分钟再灌注）。在止血带（TQ）充气和再灌注开始后30分钟收集横肌活检。蛋白质印迹分析在肌肉蛋白中进行4-HNE，SOD2,TNF-α,IL-6,p-Drp1ser616,Drp1,Mfn1,Mfn2,Opa1,PGC-1,ETC复杂I-V，细胞色素c,切割的胱天蛋白酶-3和胱天蛋白酶-3。术前和术后评估临床结果，包括等速肌力和生活质量。
UNASSIGNED：IPC显着增加Mfn2（2.0±0.2vs1.2±0.1，p=0.001）和Opa1（2.9±0.3vs1.9±0.2，p=0.005）在再灌注开始时的蛋白质表达，与缺血期相比。4-HNE没有差异，SOD2,TNF-α,IL-6,p-Drp1ser616/Drp1,Mfn1,PGC-1α,ETC复杂I-V，细胞色素c,缺血和再灌注期之间caspase-3/caspase-3的表达，或群体之间。临床上,假IPC组术后膝关节伸展最大扭矩显著降低(-16.6[-29.5,-3.6]N.m,p=0.020)，而IPC组中的保留（-4.7[-25.3，16.0]N.m，p=0.617）。
未经评估：在带有TQ应用程序的TKA中，IPC保留了术后股四头肌的力量，并部分通过增强骨骼肌中的线粒体融合蛋白来防止TQ引起的I/R损伤。
UASSIGNED：线粒体融合是IPC预防骨骼肌I/R损伤的潜在潜在潜在机制。在TQ诱导的I/R之前应用IPC保留了TKA术后股四头肌肌力。
UNASSIGNED: Tourniquet-induced ischemia and reperfusion (I/R) has been related to postoperative muscle atrophy through mechanisms involving protein synthesis/breakdown, cellular metabolism, mitochondrial dysfunction, and apoptosis. Ischemic preconditioning (IPC) could protect skeletal muscle against I/R injury. This study aims to determine the underlying mechanisms of IPC and its effect on muscle strength after total knee arthroplasty (TKA).
UNASSIGNED: Twenty-four TKA patients were randomized to receive either sham IPC or IPC (3 cycles of 5-min ischemia followed by 5-min reperfusion). Vastus medialis muscle biopsies were collected at 30 min after tourniquet (TQ) inflation and the onset of reperfusion. Western blot analysis was performed in muscle protein for 4-HNE, SOD2, TNF-ɑ, IL-6, p-Drp1ser616, Drp1, Mfn1, Mfn2, Opa1, PGC-1ɑ, ETC complex I-V, cytochrome c, cleaved caspase-3, and caspase-3. Clinical outcomes including isokinetic muscle strength and quality of life were evaluated pre- and postoperatively.
UNASSIGNED: IPC significantly increased Mfn2 (2.0 ± 0.2 vs 1.2 ± 0.1, p = 0.001) and Opa1 (2.9 ± 0.3 vs 1.9 ± 0.2, p = 0.005) proteins expression at the onset of reperfusion, compared to the ischemic phase. There were no differences in 4-HNE, SOD2, TNF-ɑ, IL-6, p-Drp1ser616/Drp1, Mfn1, PGC-1ɑ, ETC complex I-V, cytochrome c, and cleaved caspase-3/caspase-3 expression between the ischemic and reperfusion periods, or between the groups. Clinically, postoperative peak torque for knee extension significantly reduced in the sham IPC group (-16.6 [-29.5, -3.6] N.m, p = 0.020), while that in the IPC group was preserved (-4.7 [-25.3, 16.0] N.m, p = 0.617).
UNASSIGNED: In TKA with TQ application, IPC preserved postoperative quadriceps strength and prevented TQ-induced I/R injury partly by enhancing mitochondrial fusion proteins in the skeletal muscle.
UNASSIGNED: Mitochondrial fusion is a potential underlying mechanism of IPC in preventing skeletal muscle I/R injury. IPC applied before TQ-induced I/R preserved postoperative quadriceps muscle strength after TKA.
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