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Bupivacaine-induced Apoptosis in the Primary Cultured Cardiomyocytes via p38 MAPKs
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Kim, Hyun Jeong | - |
dc.contributor.author | Sung, Se Ra | - |
dc.contributor.author | Seo, Kwang Suk | - |
dc.contributor.author | Lim, Seung Woon | - |
dc.contributor.author | Yoon, Tae Gyoon | - |
dc.date.accessioned | 2011-10-19T06:02:13Z | - |
dc.date.available | 2011-10-19T06:02:13Z | - |
dc.date.issued | 2006-06 | - |
dc.identifier.citation | Kor J Anesth 2006;50:S48-56 | en |
dc.identifier.issn | 2005-6419 | - |
dc.identifier.uri | https://hdl.handle.net/10371/74332 | - |
dc.description.abstract | Background: It is known that bupivacaine induce cell death in several immortalized cells. However, there is no report
concerning bupivacaine-induced cell death in the primary cultured cardiomyocytes. We compared the direct cytotoxicity of local anesthetics in cardiomyocytes. Furthermore, the mechanisms of cell death were evaluated. Methods: The myocardial cells of rat pups were cultured 3 days after seeding. The methyltetrazolium (MTT) assay was employed to quantify differences in cellular viability. To confirm apoptosis, Hoechst-propidium iodide staining, DNA fragmentation by electrophoresis and western blot analysis were performed. And to examine the mechanisms of cell death, intracellular calcium and expression levels of mitogen-activated protein kinases (MAPKs) family members were evaluated. Results: Among the local anesthetics under 1 mM concentration for 18 h, only bupivacaine significantly decreased the MTT activity (P < 0.001). Bupivacaine induced cell death in a dose-responsive and time dependent manner. Cell death showed apoptotic characteristics, such as DNA fragmentation, chromatin condensation, decrease of precursor caspase-3 protein level, increased cleaved PARP, and cytochrome C release into the cytoplasm. Bupivacaine phosphorylated three major MAPKs, i.e. extracellular signalregulated kinases (ERKs), p38 kinase and c-Jun N-terminal kinases (JNKs) stress-activated protein kinases. Administration of ERK inhibitor increase cell death, whereas inhibitors of p38 kinase and JNK decreased cell death (P < 0.05). In addition, the intracellular calcium level was approximately 4 times higher after the bupivacaine treatment (P < 0.001), which was inhibited by calcium chelators (P < 0.001). Calcium chelators inhibited expression of MAPKs. Conclusions: In bupivacaine-induced apoptosis in cardiomyocytes, intracellular calcium increase and MAPKs family plays important roles. | en |
dc.language.iso | en | en |
dc.publisher | 대한마치과학회 | en |
dc.subject | apoptosis | en |
dc.subject | bupivacaine | en |
dc.subject | calcium | en |
dc.subject | cardiomyocyte | en |
dc.subject | levobupivacaine | en |
dc.subject | mitogen-activated protein kinases | en |
dc.title | Bupivacaine-induced Apoptosis in the Primary Cultured Cardiomyocytes via p38 MAPKs | en |
dc.type | Article | en |
dc.contributor.AlternativeAuthor | 김현정 | - |
dc.contributor.AlternativeAuthor | 성세라 | - |
dc.contributor.AlternativeAuthor | 서광석 | - |
dc.contributor.AlternativeAuthor | 임승운 | - |
dc.contributor.AlternativeAuthor | 윤태균 | - |
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