ERKs and mitochondria-related pathways are essential for glycyrrhizic acid-mediated neuroprotection against glutamate-induced toxicity in differentiated PC12 cells
In: Brazilian Journal of Medical and Biological Research, Jg. 47 (2014-09-01), Heft 9
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Zugriff:
The present study focuses on the neuroprotective effect of glycyrrhizic acid (GA, a major compound separated from Glycyrrhiza Radix, which is a crude Chinese traditional drug) against glutamate-induced cytotoxicity in differentiated PC12 (DPC12) cells. The results showed that GA treatment improved cell viability and ameliorated abnormal glutamate-induced alterations in mitochondria in DPC12 cells. GA reversed glutamate-suppressed B-cell lymphoma 2 levels, inhibited glutamate-enhanced expressions of Bax and cleaved caspase 3, and reduced cytochrome C (Cyto C) release. Exposure to glutamate strongly inhibited phosphorylation of AKT (protein kinase B) and extracellular signal-regulated kinases (ERKs); however, GA pretreatment enhanced activation of ERKs but not AKT. The presence of PD98059 (a mitogen-activated protein/extracellular signal-regulated kinase kinase [MEK] inhibitor) but not LY294002 (a phosphoinositide 3-kinase [PI3K] inhibitor) diminished the potency of GA for improving viability of glutamate-exposed DPC12 cells. These results indicated that ERKs and mitochondria-related pathways are essential for the neuroprotective effect of GA against glutamate-induced toxicity in DPC12 cells. The present study provides experimental evidence supporting GA as a potential therapeutic agent for use in the treatment of neurodegenerative diseases.
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ERKs and mitochondria-related pathways are essential for glycyrrhizic acid-mediated neuroprotection against glutamate-induced toxicity in differentiated PC12 cells
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Autor/in / Beteiligte Person: | Wang, D. ; Guo, T.Q. ; Wang, Z.Y. ; Lu, J.H. ; Liu, D.P. ; Meng, Q.F. ; Xie, J. ; Zhang, X.L. ; Liu, Y. ; Teng, L.S. |
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Zeitschrift: | Brazilian Journal of Medical and Biological Research, Jg. 47 (2014-09-01), Heft 9 |
Veröffentlichung: | Associação Brasileira de Divulgação Científica, 2014 |
Medientyp: | academicJournal |
ISSN: | 0100-879X (print) |
DOI: | 10.1590/1414-431X20143760 |
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