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Artemisinin conferred ERK mediated neuroprotection to PC12 cells and cortical neurons exposed to sodium nitroprusside-induced oxidative insult
Zheng W.2; Chong C.-M.2; Wang H.2; Zhou X.2; Zhang L.2; Wang R.2; Meng Q.2; Lazarovici P.3; Fang J.2
2016-08-01
Source PublicationFree Radical Biology and Medicine
ISSN18734596 08915849
Volume97Pages:158-167
Abstract

The production of nitric oxide (NO) is one of the primary mediators of ischemic damage, glutamate neurotoxicity and neurodegeneration and therefore inhibition of NO-induced neurotoxicity may be considered a therapeutic target for reducing neuronal cell death (neuroprotection). In this study, artemisinin, a well-known anti-malaria drug was found to suppress sodium nitroprusside (SNP, a nitric oxide donor)-induced cell death in the PC12 cells and brain primary cortical neuronal cultures. Pretreatment of PC12 cells with artemisinin significantly suppressed SNP-induced cell death by decreasing the extent of oxidation, preventing the decline of mitochondrial membrane potential, restoring abnormal changes in nuclear morphology and reducing lactate dehydrogenase release and inhibiting caspase 3/7 activities. Western blotting analysis revealed that artemisinin was able to activate extracellular regulated protein kinases (ERK) pathway. Furthermore, the ERK inhibitor PD98059 blocked the neuroprotective effect of artemisinin whereas the PI3K inhibitor LY294002 had no effect. Cumulatively these findings support the notion that artemisinin confers neuroprotection from SNP-induce neuronal cell death insult, a phenomenon coincidentally related to activation of ERK phosphorylation. This SNP-induced oxidative insult in PC12 cell culture model may be useful to investigate molecular mechanisms of NO-induced neurotoxicity and drug-induced neuroprotection, and to generate novel therapeutic concepts for ischemic disease treatment.

KeywordArtemisinin Erk1/2 Neuroprotection Pc12 Cells Sodium Nitroprusside
DOI10.1016/j.freeradbiomed.2016.05.023
URLView the original
Indexed BySCI
Language英语
WOS Research AreaBiochemistry & Molecular Biology ; Endocrinology & Metabolism
WOS SubjectBiochemistry & Molecular Biology ; Endocrinology & Metabolism
WOS IDWOS:000381924100014
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被引频次[WOS]:21   [WOS记录]     [WOS相关记录]
Document TypeJournal article
专题Faculty of Health Sciences
Institute of Chinese Medical Sciences
Corresponding AuthorZheng W.
Affiliation1.Zhongshan Ophthalmic Center
2.Universidade de Macau
3.Hebrew University of Jerusalem
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Zheng W.,Chong C.-M.,Wang H.,et al. Artemisinin conferred ERK mediated neuroprotection to PC12 cells and cortical neurons exposed to sodium nitroprusside-induced oxidative insult[J]. Free Radical Biology and Medicine,2016,97:158-167.
APA Zheng W..,Chong C.-M..,Wang H..,Zhou X..,Zhang L..,...&Fang J..(2016).Artemisinin conferred ERK mediated neuroprotection to PC12 cells and cortical neurons exposed to sodium nitroprusside-induced oxidative insult.Free Radical Biology and Medicine,97,158-167.
MLA Zheng W.,et al."Artemisinin conferred ERK mediated neuroprotection to PC12 cells and cortical neurons exposed to sodium nitroprusside-induced oxidative insult".Free Radical Biology and Medicine 97(2016):158-167.
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