Abstract:
AIM:To investigate possible intracellular signal molecules involved in diphenylhydantoin (DPH)-mediated apoptosis of cerebellar granule neurons (CGN) and explore possible molecular mechanisms of neurotoxicity of DPH. METHODS:Fluorescein diacetate (FDA) stain, hochest 33258 stain, and agar gel electrophoresis were used to test morphological and biological characters of primary CGN and cortical neurons (CN) in the presence or absence of 100 micromol/L DPH; Western blot and RT-PCR were employed to further investigate apoptotic/survival signal moleculars involved in the neuronal apoptotic signal transdution. RESULTS:DPH 100 micromol/L induced a typical apoptosis of CGN but had no toxicity on CN. Cerebellar granule neural apoptosis induced by 100 micromol/L DPH was significantly inhibited by pre-treatment with SB203580 (10 micromol/L) or CEP-11004 (1 micromol/L) for 1 h. DPH markedly upregulated the levels of phospho-c-Jun (active c-Jun), total c-Jun protein and c-jun mRNA in CGN. The levels of phospho-c-Jun dramatically elevated by DPH at 8 h were significantly inhibited by SB203580 (10 micromol/L) or CEP-11004 (1 micromol/L). Moreover, the activities of p44/42 (ERK1/ERK2), other members of MAP kinases and generally believed to be important survival effetors in CGN, were markedly suppressed. However, the activities of both JNK and p38 were little affected in the process of apoptosis of CGN induced by 100 micromol/L DPH. CONCLUSION:The selective toxicity of DPH on CGN is likely due to its ability to induce apoptosis of CGN, it is a process involved activation of c-Jun and suppression of the activity of p44/42.
journal_name
Acta Pharmacol Sinjournal_title
Acta pharmacologica Sinicaauthors
Zhao LZ,Su XW,Huang YJ,Qiu PX,Yan GMsubject
Has Abstractpub_date
2003-06-01 00:00:00pages
539-48issue
6eissn
1671-4083issn
1745-7254journal_volume
24pub_type
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journal_title:Acta pharmacologica Sinica
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doi:
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doi:
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更新日期:2004-06-01 00:00:00
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更新日期:2002-04-01 00:00:00
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更新日期:2018-06-01 00:00:00
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