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Dexamethasone Attenuates Bupivacaine-induced Neuron Injury Through Akt-dependent Mechanism

Author: MaRong
Tutor: DingZhengNian
School: Nanjing Medical University
Course: Anesthesiology
Keywords: Local anesthetics Dexamethasone Neurotoxicity Akt
CLC: R614
Type: Master's thesis
Year: 2009
Downloads: 19
Quote: 0
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Abstract


Local anesthetics may result in neuron injury and can even cause neurological complications. In this study, the effect of dexamethasone on the toxicity of bupivacaine (a clinic widely used local anesthetics) in mouse neuroblastoma N2a cells was investigated. The results revealed that bupivacaine induced significant N2a cell injuries as evidenced by cellular morphological changes, increased LDH leakage and nuclei condensation. Dexamethasone attenuated all of these changes. It was also found that bupivacaine-induced N2a cell toxicity involving the decline of mitochondrial transmembrane potential and dephosphorylation of Akt, while both of them were better maintained when the cells pretreated with dexamethasone. Moreover, inhibition of Akt activation with triciribine, a specific inhibitor of Akt phosphorylation, could remove the protective effect of dexamethasone against bupivacaine-induced N2a cell injury. These results suggest that dexamethasone attenuates bupivacaine-induced neuron injury via, in part, an Akt-dependent pathway.

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