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Tanshinone IIA Inhibits Glutamate-Induced Oxidative Toxicity through Prevention of Mitochondrial Dysfunction and Suppression of MAPK Activation in SH-SY5Y Human Neuroblastoma Cells
Joint Authors
Li, Haifeng
Shi, Ruona
Ding, Fei
Wang, Hongyu
Han, Wenjing
Huang, Zebo
Xiao, Lingyun
Ai, Liping
Source
Oxidative Medicine and Cellular Longevity
Issue
Vol. 2017, Issue 2017 (31 Dec. 2017), pp.1-13, 13 p.
Publisher
Hindawi Publishing Corporation
Publication Date
2017-06-11
Country of Publication
Egypt
No. of Pages
13
Main Subjects
Abstract EN
Glutamate excitotoxicity is associated with many neurological diseases, including cerebral ischemia and neurodegenerative diseases.
Tanshinone IIA, a diterpenoid naphthoquinone from Salvia miltiorrhiza, has been shown to suppress presynaptic glutamate release, but its protective mechanism against glutamate-induced neurotoxicity is lacking.
Using SH-SY5Y human neuroblastoma cells, we show here that excessive glutamate exposure decreases cell viability and proliferation and increases LDH release.
Pretreatment with tanshinone IIA, however, prevents the decrease in cell viability and proliferation and the increase in LDH release induced by glutamate.
Tanshinone IIA also attenuates glutamate-induced oxidative stress by reducing reactive oxygen species level and malondialdehyde and protein carbonyl contents and by enhancing activities and protein levels of superoxide dismutase and catalase.
We then show that tanshinone IIA prevents glutamate-induced mitochondrial dysfunction by increasing mitochondrial membrane potential and ATP content and by reducing mitochondrial protein carbonyl content.
Moreover, tanshinone IIA can inhibit glutamate-induced apoptosis through regulation of apoptosis-related protein expression and MAPK activation, including elevation of Bcl-2 protein level, decrease in Bax and cleaved caspase-3 levels, and suppression of JNK and p38 MAPK activation.
Collectively, our findings demonstrate that tanshinone IIA protects SH-SY5Y cells against glutamate toxicity by reducing oxidative stress and regulating apoptosis and MAPK pathways.
American Psychological Association (APA)
Li, Haifeng& Han, Wenjing& Wang, Hongyu& Ding, Fei& Xiao, Lingyun& Shi, Ruona…[et al.]. 2017. Tanshinone IIA Inhibits Glutamate-Induced Oxidative Toxicity through Prevention of Mitochondrial Dysfunction and Suppression of MAPK Activation in SH-SY5Y Human Neuroblastoma Cells. Oxidative Medicine and Cellular Longevity،Vol. 2017, no. 2017, pp.1-13.
https://search.emarefa.net/detail/BIM-1194727
Modern Language Association (MLA)
Li, Haifeng…[et al.]. Tanshinone IIA Inhibits Glutamate-Induced Oxidative Toxicity through Prevention of Mitochondrial Dysfunction and Suppression of MAPK Activation in SH-SY5Y Human Neuroblastoma Cells. Oxidative Medicine and Cellular Longevity No. 2017 (2017), pp.1-13.
https://search.emarefa.net/detail/BIM-1194727
American Medical Association (AMA)
Li, Haifeng& Han, Wenjing& Wang, Hongyu& Ding, Fei& Xiao, Lingyun& Shi, Ruona…[et al.]. Tanshinone IIA Inhibits Glutamate-Induced Oxidative Toxicity through Prevention of Mitochondrial Dysfunction and Suppression of MAPK Activation in SH-SY5Y Human Neuroblastoma Cells. Oxidative Medicine and Cellular Longevity. 2017. Vol. 2017, no. 2017, pp.1-13.
https://search.emarefa.net/detail/BIM-1194727
Data Type
Journal Articles
Language
English
Notes
Includes bibliographical references
Record ID
BIM-1194727