8 research outputs found
Modulatory effects of nitric oxide-active drugs on the anticonvulsant activity of lamotrigine in an experimental model of partial complex epilepsy in the rat-4
<p><b>Copyright information:</b></p><p>Taken from "Modulatory effects of nitric oxide-active drugs on the anticonvulsant activity of lamotrigine in an experimental model of partial complex epilepsy in the rat"</p><p>BMC Neuroscience 2007;8():47-47.</p><p>Published online 3 Jul 2007</p><p>PMCID:PMC1950521.</p><p></p>ogressive number of train of stimuli applied every 10 min is indicated. The chi-square test was used to compare the animals responding and not responding to the electrical stimulation. The differences were considered marginally and highly significant at the level of P < 0.05 (*) and P < 0.005 (**) respectively
Modulatory effects of nitric oxide-active drugs on the anticonvulsant activity of lamotrigine in an experimental model of partial complex epilepsy in the rat-1
<p><b>Copyright information:</b></p><p>Taken from "Modulatory effects of nitric oxide-active drugs on the anticonvulsant activity of lamotrigine in an experimental model of partial complex epilepsy in the rat"</p><p>BMC Neuroscience 2007;8():47-47.</p><p>Published online 3 Jul 2007</p><p>PMCID:PMC1950521.</p><p></p>10 rats for each treatment). In abscissa the progressive number of train of stimuli applied every 10 min is indicated. Asterisks between lines (-*-) indicate a significant difference between the two treatments (P < 0.05)
Image_1_Brain Distribution and Modulation of Neuronal Excitability by Indicaxanthin From Opuntia Ficus Indica Administered at Nutritionally-Relevant Amounts.JPEG
<p>Several studies have recently investigated the role of nutraceuticals in complex pathophysiological processes such as oxidative damages, inflammatory conditions and excitotoxicity. In this regard, the effects of nutraceuticals on basic functions of neuronal cells, such as excitability, are still poorly investigated. For this reason, the possible modulation of neuronal excitability by phytochemicals (PhC) could represent an interesting field of research given that excitotoxicity phenomena are involved in neurodegenerative alterations leading, for example, to Alzheimer’s disease. The present study was focused on indicaxanthin from Opuntia ficus indica, a bioactive betalain pigment, with a proven antioxidant and anti-inflammatory potential, previously found to cross blood-brain barrier (BBB) and to modulate the bioelectric activity of hippocampal neurons. On this basis, we aimed at detecting the specific brain areas where indicaxanthin localizes after oral administration at dietary-achievable amounts and highlighting eventual local effects on the excitability of single neuronal units. HPLC analysis of brain tissue 1 h after ingestion of 2 μmol/kg indicaxanthin indicated that the phytochemical accumulates in cortex, hippocampus, diencephalon, brainstem and cerebellum, but not in the striato-pallidal complex. Then, electrophysiological recordings, applying the microiontophoretic technique, were carried out with different amounts of indicaxanthin (0.34, 0.17, 0.085 ng/neuron) to assess whether indicaxanthin influenced the neuronal firing rate. The data showed that the bioelectric activity of neurons belonging to different brain areas was modulated after local injection of indicaxanthin, mainly with dose-related responses. A predominating inhibitory effect was observed, suggesting a possible novel beneficial effect of indicaxanthin in reducing cell excitability. These findings can constitute a new rationale for exploring biological mechanisms through which PhC could modulate neuronal function with a relapse on complex cognitive brain process and related neurodegenerative conditions.</p
Spheres formation, cytometric analysis and telomerase activity.
<p>(A) Sphere clusters formed by CD34<sup>+</sup>/CD90<sup>+</sup> cells in semisolid medium after 24 hours (Original Magnification×100); (B) Cytometric analysis on adherent cells for CD90 (80%) and CD34 (80%) antigens and on floating spheres for CD90 (2–3%) and CD34 (95–98%) antigens; (C) Telomerase activity of differentiated endothelial cells (ΔA = 0.160) was significantly reduced (p<0.001) respect to undifferentiated CD34<sup>+</sup>/CD90<sup>+</sup> cells (ΔA = 0.377)</p
Cell cycle analysis performed using Hoechst 33342 and Ki67 both on CD34 negative and positive cells.
<p>(A) Hoechst 33342 analysis performed CD34<sup>−</sup> cells: G<sub>0</sub>G<sub>1</sub> phase (98%), S phase (0,65%) and G<sub>2</sub>M phase (0,50%); (B) Ki67 analysis performed CD34- cells: Ki67 (10%); (C) Hoechst 33342 analysis performed CD34<sup>+</sup> cells: G<sub>0</sub>G<sub>1</sub> phase (84%), S phase (5%) and G<sub>2</sub>M phase (10%); (D) Ki67 analysis performed CD34+ cells: Ki67 (85%).</p
RT-PCR analysis.
<p>(A) Representative figure of RT-PCR showing mRNA transcript expression of CD90, CD34, CD44, CD54, VEGF, Flk-1, on cells in DMEM 10% FBS 7, 15 and 30 days of culture; (B) PPARγ and adiponectin on cells in adipogenic medium at 7 and (C) 30 days of culture.</p
Adipogenic differentiation.
<p>(A) ASCs in DMEM 10% FBS exhibit a fibroblast-like morphology (Original magnification 100×); (B) ASCs in adipogenic medium exhibit an adipocyte morphology (Original magnification 100×); (C) CD34<sup>+</sup>/CD90<sup>+</sup> cells in DMEM 10% FBS showing negativity for adiponectin by immunohistochemistry (Original magnification 400×); (D) CD34<sup>+</sup>/CD90<sup>+</sup> cells in adipogenic medium showing positivity for adiponectin by immunohistochemistry (Original magnification 100×); (E) CD34<sup>−</sup>/CD90<sup>−</sup> cells in DMEM 10% FBS showing negativity for adiponectin by immunohistochemistry (Original magnification 100×); (F) CD34<sup>−</sup>/CD90<sup>−</sup> cells in adipogenic medium showing negativity for adiponectin by immunohistochemistry (Original magnification 400×).</p
Representative flow cytometry analysis performed on CD34<sup>+</sup>/CD90<sup>+</sup> cells at day 30 from sorting.
<p>A significant number of ASCs are clearly positive for endothelial markers, including CD90 (97%), CD44 (90%), CD54 (90%), VEGF (70%), CD133 (18%), and Flk-1 (60%). Control PE-conjugated and FITC-conjugated isotypes were negative.</p