کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9429410 | 1297042 | 2005 | 5 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Stepholidine protects against H2O2 neurotoxicity in rat cortical neurons by activation of Akt
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موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
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چکیده انگلیسی
The fundamental pathological process(es) associated with schizophrenia (SZ) remain(s) uncertain, but multiple lines of evidence suggest that this condition is associated with excessive stimulation of striatal dopamine (DA) D2 receptors, deficient stimulation of medial prefrontal cortex (mPFC) D1 receptors as well as neuronal apoptosis. Unlike typical antipsychotics, stepholidine (SPD), which is isolated from the Chinese herb stephania, has D1 and D2 dual properties and regulates neuronal cell differentiation and proliferation. It is unknown, however, whether it possesses a neuroprotective property. Here, we report that SPD prevented neuronal cell death from H2O2 exposure and increased the levels of phosphorylated Akt (pAkt), a serine/threonine protein kinase. The SPD-induced neuroprotection and activation of Akt were blocked by LY294002, a PI3-K inhibitor, suggesting that the anti-apoptotic action of SPD is mediated via the PI3-K/Akt signaling pathway. Thus, as a survival or anti-apoptotic factor for neuronal cells, SPD may contribute to the therapeutic action of SPD in SZ treatment.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience Letters - Volume 383, Issue 3, 5 August 2005, Pages 328-332
Journal: Neuroscience Letters - Volume 383, Issue 3, 5 August 2005, Pages 328-332
نویسندگان
Lei Zhang, Rulun Zhou, Guoqiang Xiang,