Abstract:
: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.
journal_name
Neurosci Lettjournal_title
Neuroscience lettersauthors
Zhang L,Zhou R,Xiang Gdoi
10.1016/j.neulet.2005.04.016keywords:
subject
Has Abstractpub_date
2005-08-05 00:00:00pages
328-32issue
3eissn
0304-3940issn
1872-7972pii
S0304-3940(05)00403-9journal_volume
383pub_type
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