Abstract:
:Catalpol has been shown to rescue neurons from kinds of damage in vitro and in vivo in previous reports. However, the effect of catalpol on the nitric oxide (NO) system via MAPKs signaling pathway of mesencephalic neurons largely remains to be verified. The current study examined that whether catalpol modulated NO and iNOS increase by rotenone in primary mesencephalic neurons and investigated its underlying signaling pathways. Present results indicated that catalpol inhibited primary mesencephalic neurons from apoptosis by morphological assay, immunocytochemistry and flow cytometric evaluation. Moreover, the ERK signaling pathway plays an important role in NO-mediated degeneration of neuron. The current results suggest that catalpol is a potential agent for the prevention of neurons apoptosis by regulating NO and iNOS increase in ERK-mediated neurodegenerative disorders.
journal_name
Neurochem Intjournal_title
Neurochemistry internationalauthors
Bi J,Jiang B,Hao S,Zhang A,Dong Y,Jiang T,An Ldoi
10.1016/j.neuint.2008.12.003subject
Has Abstractpub_date
2009-03-01 00:00:00pages
264-70issue
3-4eissn
0197-0186issn
1872-9754pii
S0197-0186(08)00195-2journal_volume
54pub_type
杂志文章abstract::The iron siderophore binding protein lipocalin 2 (LCN2, also known as 24p3, NGAL and siderocalin) may be involved in iron homeostasis, but to date, little is known about expression of its putative receptor, brain-type organic cation transporter (BOCT, also known as BOCT1, 24p3R, NGALR and LCN2R), in the brain during n...
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journal_title:Neurochemistry international
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journal_title:Neurochemistry international
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journal_title:Neurochemistry international
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journal_title:Neurochemistry international
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journal_title:Neurochemistry international
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