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缺血再灌注后大鼠骨骼肌中生化标志物水平和核数的改变。

Alterations of biochemical marker levels and myonuclear numbers in rat skeletal muscle after ischemia-reperfusion.

机构信息

Department of Integrative Physiology, Gunma University Graduate School of Medicine, 3-39-22, Maebashi, Gunma 371-8511, Japan.

出版信息

Mol Cell Biochem. 2013 Jan;373(1-2):11-8. doi: 10.1007/s11010-012-1470-0. Epub 2012 Oct 13.

DOI:10.1007/s11010-012-1470-0
PMID:23065010
Abstract

Prolonged ischemia-reperfusion results in various damages in skeletal muscle. Following reperfusion, although the damaged muscles undergo regeneration, the precise process and mechanism of regeneration have not yet been fully understood. Here, we show the altered levels of plasma biochemical markers of muscle damage, and the change in myonuclear numbers in adult rat skeletal muscle by ischemia-reperfusion. Male Wistar rats were subjected to unilateral hindlimb ischemia by clamping the anterior tibial artery for 2 h before reperfusion. Both plasma creatine kinase activity and C-reactive protein levels in plasma were increased significantly at 0.5 h of reperfusion and returned to the control level at 24 h. The transverse sectional area of muscle belly of the anterior tibial muscles in ischemic side was significantly decreased by 20 % compared with those in sham-ischemic (control) side at 2 days, and returned to the control level at 5 days of reperfusion. Moreover, the number of interstitial nuclei in the ischemic side were significantly increased at 5-14 days and returned to the control level at 21 days of reperfusion. Central nuclei that are specifically observed in regenerating muscle, appeared at 5 days, reached a peak at 14 days, and disappeared at 28 days of reperfusion. Furthermore, MyoD, a regulatory factor for myogenesis, showed a transient expression at 5 days of reperfusion. These results indicate that, although the size of muscle seems to be recovered by 5 days of reperfusion, the most active muscle regeneration occurs much later, as shown by the increase in central nuclei.

摘要

长时间的缺血再灌注会导致骨骼肌的各种损伤。再灌注后,虽然受损的肌肉会经历再生,但再生的确切过程和机制尚未完全清楚。在这里,我们展示了缺血再灌注后成年大鼠骨骼肌中血浆肌肉损伤生化标志物水平的变化和核数的变化。雄性 Wistar 大鼠通过在前胫骨动脉夹闭 2 小时来进行单侧后肢缺血,然后再进行再灌注。再灌注 0.5 小时后,血浆肌酸激酶活性和 C 反应蛋白水平显著升高,并在 24 小时内恢复到对照水平。与假缺血(对照)侧相比,缺血侧前胫骨肌的肌腹横截面积在 2 天显著减少了 20%,并在 5 天的再灌注时恢复到对照水平。此外,缺血侧的间质核数量在 5-14 天显著增加,并在 21 天的再灌注时恢复到对照水平。在再生肌肉中特异性观察到的中央核在 5 天出现,在 14 天达到峰值,并在 28 天的再灌注时消失。此外,肌生成的调节因子 MyoD 在再灌注 5 天时表现出短暂的表达。这些结果表明,尽管肌肉大小似乎在再灌注 5 天内得到恢复,但最活跃的肌肉再生发生在更晚的时间,如中央核的增加所示。

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