The Effects of Hispidulin on Bupivacaine-Induced Neurotoxicity: Role of AMPK Signaling Pathway

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• 作者：Xinhuan Niu (1)
  Jie Chen (2)
  Ping Wang (1)
  Hui Zhou (1)
  Song Li (1)
  Mengyuan Zhang (1)
  
• 关键词：Bupivacaine ; Hispidulin ; Neurotoxicity ; AMPK
• 刊名：Cell Biochemistry and Biophysics
• 出版年：2014
• 出版时间：September 2014
• 年：2014
• 卷：70
• 期：1
• 页码：241-249
• 全文大小：1,923 KB
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• 作者单位：Xinhuan Niu (1)
  Jie Chen (2)
  Ping Wang (1)
  Hui Zhou (1)
  Song Li (1)
  Mengyuan Zhang (1)
  
  1. Department of Anesthesiology, Shandong Provincial Hospital, Shandong University, No.324, JingWu Road, Jinan, 250021, China
  2. Department of General Surgery, People’s Hospital of Huai Yin District, Jinan, 250021, China
  
• ISSN：1559-0283

文摘

Bupivacaine is a sodium channel blocker, which is widely used for local infiltration nerve block, epidural and intrathecal anesthesia. However, bupivacaine could cause nerve damage. Hispidulin was shown to be able to penetrate the blood–brain barrier and possess antiepileptic activity. In this study, we investigate whether hispidulin administration could attenuate bupivacaine-induced neurotoxicity. Bupivacaine-challenged mouse neuroblastoma N2a cells were treated with hispidulin. The neuron injury was assessed by examination of cell viability and apoptosis. The levels of activation of AMP-activated protein kinase (AMPK) signaling pathway were examined along with the effect of blocking AMPK signaling on cell viability in the presence of hispidulin and bupivacaine. Our results showed that Bupivacaine treatment significantly decreased cell viability and induced apoptosis. Treatment with hispidulin significantly attenuated bupivacaine-induced cell injury. In addition, hispidulin treatment increased the levels of phospho-AMPK and phospho-GSK3β and attenuated bupivacaine-induced loss in mitochondrial membrane potential. Furthermore, we found that blocking AMPK signaling pathway significantly abolished the cytoprotective effect of hispidulin against bupivacaine-induced cell injury. Our findings suggest that treatment of neuroblastoma cells with hispidulin-protected neural cells from Bupivacaine-induced injury via the activation of the AMPK/GSK3β signaling pathway.