| Literature DB >> 20128049 |
Li Li1, Hao-Jan Tsai, Lin Li, Xue-Mei Wang.
Abstract
Overload of intracellular calcium caused by amyloid-beta peptide has been implicated in the pathogenesis of neuronal damage in Alzheimer's disease. Voltage-gated calcium channels (VGCCs) provide one of the major sources of Ca(2+) entry into cells. Here, we investigated whether icariin had effect on the changes of calcium currents induced by Abeta(25-35) in hippocampal pyramidal neurons. Using whole-cell patch-clamp, we showed that Abeta(25-35) enhanced the inward Ba(2+) and Ca(2+) currents. The currents were partially inhibited by Ni(2+) and completely suppressed by Cd(2+), indicating that Abeta(25-35) disrupts intracellular calcium homeostasis via the modulation of both L- and T-type channels. Furthermore, icariin nearly complete suppressed the abnormal inward calcium currents induced by Abeta(25-35) in a dose-dependant manner. Our findings suggest that the potential neuroprotective effect of icariin on Abeta(25-35)-induced neurotoxicity via the balance intracelluar calcium homeostasis.Entities:
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Year: 2010 PMID: 20128049 DOI: 10.1142/S0192415X10007701
Source DB: PubMed Journal: Am J Chin Med ISSN: 0192-415X Impact factor: 4.667