Icariin Inhibits the Increased Inward Calcium Currents Induced by Amyloid-β_25-35 Peptide in CA1 Pyramidal Neurons of Neonatal Rat Hippocampal Slice

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.

Fermented Herbal Formulas KIOM-MA128 Ameliorate IL-6-Induced Intestinal Barrier Dysfunction in Colon Cancer Cell Line

“…Arctigenin, arctiin, and matairesinol reinforced the intestinal barrier function through the regulation of paracellular permeability [22]. Moreover, icariin inhibited permeability in sertoli cells and the regulation of TJ proteins in pyramidal neurons [23, 24]. Here, we used KIOM-MA128, the fermentation of KIOM-MA, to determine whether it facilitated improvements in the protective effects on intestinal barrier dysfunction via the inhibition of actin cytoskeletal rearrangement.…”

Natural products as a source of Alzheimer's drug leads

“…(Berberidaceae), was shown to reduce behavioral dysfunction and neurodegeneration in rat models, 393 while blocking Ca 2+ currents disrupted by Aβ25-35. 394 A synthetic derivative of the sponge ( Aplysina cavernicola Vacelet (Aplysinidae)) metabolite 11,19-dideoxyfistularin, NP04634 ( 180 ), protected neurons from calcium overload and mitochondrial disruption. Specifically, 180 protects neurons from toxicity induced by 30K + /5Ca 2+ /FPL at a concentration of 10 μM, reduces voltage dependent Ca 2+ levels and protects mitochondrial disruption by preventing depolarization.…”

Neurotransmitter receptor and time dependence of the synaptic plasticity disrupting actions of Alzheimer's disease Aβ in vivo

“…Although the relatively strong inhibition of NMDAR-independent LTP may be due to its relatively small magnitude, an alternative explanation is that Ab interferes with the function of voltage-activated Ca 2þ channels [22,23]. Ab can boost Ni 2þ -sensitive Ca 2þ channels in hippocampal pyramidal cells [24,25], which could lead to excessive or inappropriate Ca 2þ entry into the cell. On the other hand, Ab did not inhibit the function of Ni 2þ -sensitive Ca 2þ channels under the same in vitro conditions in which it inhibited hippocampal NMDAR-dependent LTP [26].…”