Carbon Monoxide Alleviates Post-ischemia-reperfusion Skeletal Muscle Injury and Systemic Inflammation.

IF 1.7 4区 医学 Q3 PHARMACOLOGY & PHARMACY
K. Taguchi, Shigeru Ogaki, Hitoshi Maeda, Yu Ishima, Hiroshi Watanabe, Masaki Otagiri, Toru Maruyama
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Abstract

Restoration of blood flow in skeletal muscle after a prolonged period of ischemia induces muscular ischemia-reperfusion injury, leading to local injury/dysfunction in muscles followed by systemic inflammatory responses. However, preventive/curative agents for skeletal muscle ischemia injury are unavailable in clinics to date. Increasing evidence has validated that carbon monoxide (CO) prevents the progression of ischemia-reperfusion injury in various organs owing to its versatile bioactivity. Previously, we developed a bioinspired CO donor, CO-bound red blood cells (CO-RBC), which mimics the dynamics of RBC-associated CO in the body. In the present study, we have tested the therapeutic potential of CO-RBC in muscular injury/dysfunction and secondary systemic inflammation induced by skeletal muscle ischemia-reperfusion. The results indicate that CO-RBC rather than RBC alone suppressed elevation of plasma creatine phosphokinase, a marker of muscular injury, in rats subjected to both hind limbs ischemia-reperfusion. In addition, the results of the treadmill walking test revealed a significantly decreased muscular motor function in RBC-treated rats subjected to both hind limbs ischemia-reperfusion than that in healthy rats, however, CO-RBC treatment facilitated sustained muscular motor functions after hind limbs ischemia-reperfusion. Furthermore, CO-RBC rather than RBC suppressed the production of tumour necrosis factor (TNF)-α and interleukin (IL)-6, which were upregulated by muscular ischemia-reperfusion. Interestingly, CO-RBC treatment induced higher levels of IL-10 compared to saline or RBC treatments. Based on these findings, we suggest that CO-RBC exhibits a suppressive effect against skeletal muscle injury/dysfunction and systemic inflammatory responses after skeletal muscle ischemia-reperfusion.
一氧化碳可缓解缺血再灌注后骨骼肌损伤和全身炎症。
骨骼肌长期缺血后血流恢复会诱发肌肉缺血再灌注损伤,导致肌肉局部损伤/功能障碍,继而引发全身炎症反应。然而,迄今为止,临床上还没有针对骨骼肌缺血损伤的预防/治疗药物。越来越多的证据证明,由于一氧化碳(CO)具有多种生物活性,它可以防止各种器官缺血再灌注损伤的进展。此前,我们开发了一种生物启发式一氧化碳供体--一氧化碳结合红细胞(CO-RBC),它模拟了红细胞在体内与一氧化碳相关的动态。在本研究中,我们测试了 CO-RBC 对骨骼肌缺血再灌注引起的肌肉损伤/功能障碍和继发性全身炎症的治疗潜力。结果表明,CO-RBC 比单独使用 RBC 能抑制双后肢缺血再灌注大鼠血浆肌酸磷酸激酶(肌肉损伤的标志物)的升高。此外,跑步机行走测试结果表明,经 RBC 处理的双后肢缺血再灌注大鼠的肌肉运动功能明显低于健康大鼠,但 CO-RBC 处理却有利于后肢缺血再灌注后肌肉运动功能的维持。此外,CO-RBC 而不是 RBC 能抑制肿瘤坏死因子(TNF)-α 和白细胞介素(IL)-6 的产生,而这两种因子在肌肉缺血再灌注后会上调。有趣的是,与生理盐水或 RBC 处理相比,CO-RBC 处理能诱导更高水平的 IL-10。基于这些发现,我们认为 CO-RBC 对骨骼肌缺血再灌注后的骨骼肌损伤/功能障碍和全身炎症反应具有抑制作用。
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来源期刊
CiteScore
3.50
自引率
5.00%
发文量
247
审稿时长
2 months
期刊介绍: Biological and Pharmaceutical Bulletin (Biol. Pharm. Bull.) began publication in 1978 as the Journal of Pharmacobio-Dynamics. It covers various biological topics in the pharmaceutical and health sciences. A fourth Society journal, the Journal of Health Science, was merged with Biol. Pharm. Bull. in 2012. The main aim of the Society’s journals is to advance the pharmaceutical sciences with research reports, information exchange, and high-quality discussion. The average review time for articles submitted to the journals is around one month for first decision. The complete texts of all of the Society’s journals can be freely accessed through J-STAGE. The Society’s editorial committee hopes that the content of its journals will be useful to your research, and also invites you to submit your own work to the journals.
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