Neurotoxicity induced by bupivacaine via T-type calcium channels in SH-SY5Y cells
| Autor: | Shiyuan Xu, Quinguo Zhang, Hongzhen Liu, Hua Liang, Hanbing Wang, Xian-Jie Wen, Chenxiang Yang |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2013 |
| Předmět: |
Cyclopropanes
Cell Survival Neurotoxins chemistry.chemical_element lcsh:Medicine Apoptosis Naphthalenes Calcium Pharmacology Gene Expression Regulation Enzymologic Calcium in biology Cell Line Calcium Channels T-Type Cytosol medicine Humans Viability assay Anesthetics Local lcsh:Science Bupivacaine Calcium metabolism Multidisciplinary Dose-Response Relationship Drug L-Lactate Dehydrogenase Voltage-dependent calcium channel Caspase 3 lcsh:R T-type calcium channel Neurotoxicity Calcium Channel Blockers medicine.disease Retraction chemistry Benzimidazoles lcsh:Q medicine.drug |
| Zdroj: | PLoS ONE, Vol 8, Iss 5, p e62942 (2013) PLoS ONE |
| ISSN: | 1932-6203 |
| Popis: | There is concern regarding neurotoxicity induced by the use of local anesthetics. A previous study showed that an overload of intracellular calcium is involved in the neurotoxic effect of some anesthetics. T-type calcium channels, which lower the threshold of action potentials, can regulate the influx of calcium ions. We hypothesized that T-type calcium channels are involved in bupivacaine-induced neurotoxicity. In this study, we first investigated the effects of different concentrations of bupivacaine on SH-SY5Y cell viability, and established a cell injury model with 1 mM bupivacaine. The cell viability of SH-SY5Y cells was measured following treatment with 1 mM bupivacaine and/or different dosages (10, 50, or 100 µM) of NNC 55-0396 dihydrochloride, an antagonist of T-type calcium channels for 24 h. In addition, we monitored the release of lactate dehydrogenase, cytosolic Ca(2+) ([Ca2+]i), cell apoptosis and caspase-3 expression. SH-SY5Y cells pretreated with different dosages (10, 50, or 100 µM) of NNC 55-0396 dihydrochloride improved cell viability, reduced lactate dehydrogenase release, inhibited apoptosis, and reduced caspase-3 expression following bupivacaine exposure. However, the protective effect of NNC 55-0396 dihydrochloride plateaued. Overall, our results suggest that T-type calcium channels may be involved in bupivacaine neurotoxicity. However, identification of the specific subtype of T calcium channels involved requires further investigation. |
| Databáze: | OpenAIRE |
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