The ameliorating effect of oroxylin A on memory impairment Nec-1s was investigated using passive avoidance and Y-maze tasks and pathological changes were identified by immunostaining and western blotting. A beta(25-35) peptide (5 nmol) was administered by intra-cerebroventricular injection. In the acute treatment study, a single dose of oroxylin A (5 mg/kg, p.o.) treated 1 h
before behavioral tests was found to significantly reverse A beta(25-35)-induced cognitive impairments based on passive avoidance and Y-maze task findings (P < 0.05). Moreover, these acute effects of oroxylin A were blocked by diazepam (1 mg/kg, i.p.), a GABAA/benzodiazepine binding site agonist (P < 0.05). On the other hand, our subchronic studies revealed that oroxylin A (1 or 5 mg/kg/day, p.o.) for 7 days ameliorated the memory impairment induced by A beta(25-35) peptide. Moreover, A beta(25-35)-induced increases in GFAP (an astroglia marker) and OX-42 (a microglia marker), and increases in NOS positive cells in the hippocampus were found to be attenuated by subchronic oroxylin A (I or 5 mg/kg/day, i.p., P < 0.05). In addition, reductions in the immunoreactivity and protein level of ChAT (a cholinergic
neuronal cell marker) in the CA3 hippocampal area induced by A beta(25-35) peptide were also attenuated by oroxylin A. Furthermore, lipid peroxidation induced by A beta(25-35) was also reduced by oroxylin A. These results suggest that the amelioration of A beta(25-35)
peptide-induced memory impairment by oroxylin A is mediated via the GABAergic neurotransmitter Lonafarnib purchase system after a single administration, or by reductions in A beta(25-35) peptide-induced astrocyte and microglia activations, NOS expression, lipid peroxidation, and increased cholinergic neurotransmission after subchronic administration. (c) 2008 Published by Elsevier Ltd.”
“Foot-and-mouth disease virus (FMDV) utilizes different cell surface macromolecules to facilitate infection of cultured cells. Virus, which is virulent for susceptible animals, infects cells via four members of the alpha(V) subclass of cellular integrins. In GBA3 contrast, tissue culture adaptation of some FMDV serotypes results in the loss of viral virulence in the animal, accompanied by the loss of virus’ ability to use integrins as receptors. These avirulent viral variants acquire positively charged amino acids on surface-exposed structural proteins, resulting in the utilization of cell surface heparan sulfate (HS) molecules as receptors. We have recently shown that FMDV serotypes utilizing integrin receptors enter cells via a clathrin-mediated mechanism into early endosomes. Acidification within the endosome results in a breakdown of the viral capsid, releasing the RNA, which enters the cytoplasm by a still undefined mechanism.
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