短暂性缺血后兔脊髓腹角中腺苷单磷酸激活的蛋白激酶的作用
Effects of adenosine monophosphate-activated kinase in the ventral horn of rabbit spinal cord after transient ischemia.
作者信息
Cho Byung Moon, Kim Woosuk, Yoo Dae Young, Jung Hyo Young, Choi Jung Hoon, Won Moo-Ho, Hwang In Koo, Moon Seung Myung
出版信息
J Spinal Cord Med. 2015 Jul;38(4):538-43. doi: 10.1179/2045772314Y.0000000198. Epub 2014 May 3.
OBJECTIVE
To investigate the effect compound C, an adenosine monophosphate-activated kinase (AMPK) inhibitor, has on motor neurons of rabbit spinal cord after ischemia/reperfusion.
DESIGN
Compound C (30 mg/kg) was administered intraperitoneally to rabbits 30 minutes before ischemia and the animals were sacrificed at 15 minutes after ischemia/reperfusion to measure lactate levels and at 72 hours after ischemia/reperfusion for morphological study.
RESULTS
The administration of compound C did not produce any significant changes in physiological parameters such as pH, arterial blood gas (PaCO(2) and PaO(2)), and blood glucose in rabbit either at 10 minutes before ischemia or at 10 minutes after reperfusion. However, the administration of compound C did significantly ameliorate lactate acidosis at 15 minutes after reperfusion. In addition, the administration of compound C significantly improved the neurological scores of the rabbits and reduced the neuronal death seen in the ventral horn of their spinal cords at 72 hours after ischemia/reperfusion.
CONCLUSIONS
Inhibition of AMPK can ameliorate the ischemia-induced neuronal death in the spinal cord via the reduction of early lactate acidosis.
目的
研究腺苷单磷酸激活的蛋白激酶（AMPK）抑制剂化合物C对兔脊髓缺血/再灌注后运动神经元的影响。
设计
在缺血前30分钟给兔腹腔注射化合物C（30毫克/千克），在缺血/再灌注后15分钟处死动物以测量乳酸水平，并在缺血/再灌注后72小时进行形态学研究。
结果
在缺血前10分钟或再灌注后10分钟，化合物C的给药对兔的生理参数如pH、动脉血气（PaCO₂和PaO₂）和血糖均未产生任何显著变化。然而，化合物C的给药在再灌注后15分钟显著改善了乳酸酸中毒。此外，化合物C的给药显著改善了兔的神经学评分，并减少了缺血/再灌注后72小时其脊髓腹角出现的神经元死亡。
结论
抑制AMPK可通过减轻早期乳酸酸中毒来改善脊髓缺血诱导的神经元死亡。
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