AMPK Attenuates Bupivacaine-induced Neurotoxicity
AMPK Attenuates Bupivacaine-induced Neurotoxicity
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DOI：
10.1177/0022034510366823
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发表时间：
2010-08-01
影响因子：
7.6
通讯作者：
Kim, H. J.
中科院分区：
文献类型：
--
作者：
Lee, S. J.;Shin, T. J.;Kim, H. J.
布比卡因作为一种长效局麻药已被广泛应用。然而，有证据强烈表明布比卡因引起细胞凋亡。AMP活化蛋白激酶（AMPK）调节代谢稳态并介导细胞保护免受应激。我们推测AMPK可能在布比卡因处理的雪旺细胞中具有细胞保护作用。为了探索这一点，我们将布比卡因应用于RT 4-D 6P 2 T雪旺细胞系。比较布比卡因作用后磷酸化AMPK的表达。布比卡因诱导细胞死亡的时间和剂量依赖性的方式[50%致死剂量（LD 50）= 316 μ M]，并增加磷酸化的AMPK表达布比卡因治疗后。AICAR（一种AMPK激活剂）减弱了布比卡因诱导的细胞毒性，而化合物C（一种AMPK抑制剂）增强了它。我们的研究结果表明，AMPK途径可能会保护雪旺细胞从布比卡因诱导的细胞毒性。
Bupivacaine has been widely used as a long-acting local anesthetic. However, evidence strongly suggests that bupivacaine causes apoptosis. AMP-activated protein kinase (AMPK) regulates metabolic homeostasis and mediates cellular protection from stress. We hypothesized that AMPK may be cytoprotective in bupivacaine-treated Schwann cells. To explore this, we applied bupivacaine to the RT4-D6P2T Schwann cell line. The expression of phosphorylated AMPK was compared after bupivacaine treatment. Bupivacaine induced cell death in a time-and dose-[50% lethal dose (LD50) = 316 mu M] dependent manner, and increased expression of phosphorylated AMPK after bupivacaine treatment. Bupivacaine-induced cytotoxicity was attenuated by AICAR (an AMPK activator), whereas compound C (an AMPK inhibitor) enhanced it. The cytoprotective effect of AICAR was reversed in the presence of iodotubercidin, an AICAR inhibitor. Our results suggest that the AMPK pathway may protect Schwann cells from bupivacaine-induced cytotoxicity.