Takemura Ai, Roy Roland R, Yoshihara Ikumi, Ishihara Akihiko
Laboratory of Cell Biology and Life Science, Graduate School of Human and Environmental Studies, Kyoto University, Kyoto, Japan.
Department of Integrative Biology and Physiology and Brain Research Institute, University of California, Los Angeles, California.
Physiol Rep. 2017 Jul;5(14). doi: 10.14814/phy2.13353.
Our aim was to determine the effects of pre- and/or postconditioning with mild hyperbaric oxygen (1.25 atmospheric pressure, 36% oxygen for 3 h/day) on the properties of the soleus muscle that was atrophied by hindlimb suspension-induced unloading. Twelve groups of 8-week-old rats were housed under normobaric conditions (1 atmospheric pressure, 20.9% oxygen) or exposed to mild hyperbaric oxygen for 2 weeks. Ten groups then were housed under normobaric conditions for 2 weeks with their hindlimbs either unloaded via suspension or not unloaded. Six groups subsequently were either housed under normobaric conditions or exposed to mild hyperbaric oxygen for 2 weeks: the suspended groups were allowed to recover under reloaded conditions (unrestricted normal cage activity). Muscle weights, cross-sectional areas of all fiber types, oxidative capacity (muscle succinate dehydrogenase activity and fiber succinate dehydrogenase staining intensity) decreased, and a shift of fibers from type I to type IIA and type IIC was observed after hindlimb unloading. In addition, mRNA levels of peroxisome proliferator-activated receptor coactivator-1 decreased, whereas those of forkhead box-containing protein O1 increased after hindlimb unloading. Muscle atrophy and decreased oxidative capacity were unaffected by either pre- or postconditioning with mild hyperbaric oxygen. In contrast, these changes were followed by a return to nearly normal levels after 2 weeks of reloading when pre- and postconditioning were combined. Therefore, a combination of pre- and postconditioning with mild hyperbaric oxygen can be effective against the atrophy and decreased oxidative capacity of skeletal muscles associated with hindlimb unloading.
我们的目的是确定用轻度高压氧(1.25个大气压,36%氧气,每天3小时)进行预处理和/或后处理对因后肢悬吊诱导卸载而萎缩的比目鱼肌特性的影响。将十二组8周龄大鼠饲养在常压条件下(1个大气压,20.9%氧气)或暴露于轻度高压氧环境2周。然后,十组大鼠在常压条件下饲养2周,其下肢要么通过悬吊卸载,要么不卸载。随后,六组大鼠要么饲养在常压条件下,要么暴露于轻度高压氧环境2周:悬吊组在重新加载条件下(无限制的正常笼内活动)恢复。后肢卸载后,肌肉重量、所有纤维类型的横截面积、氧化能力(肌肉琥珀酸脱氢酶活性和纤维琥珀酸脱氢酶染色强度)均下降,并且观察到纤维从I型向IIA型和IIC型转变。此外,后肢卸载后,过氧化物酶体增殖物激活受体γ共激活因子-1的mRNA水平下降,而含叉头框蛋白O1的mRNA水平上升。轻度高压氧的预处理和后处理均未影响肌肉萎缩和氧化能力下降。相反,当联合进行预处理和后处理时,在重新加载2周后,这些变化随后恢复到几乎正常水平。因此,轻度高压氧预处理和后处理相结合可有效对抗与后肢卸载相关的骨骼肌萎缩和氧化能力下降。