scholarly journals The Neuroprotective Effects of Astragaloside IV against H2O2-Induced Damage in SH-SY5Y Cells are Associated with Synaptic Plasticity

2020 ◽  
Vol 2020 ◽  
pp. 1-7
Author(s):  
Zurong Song ◽  
Ali Tao
Keyword(s):  
Synaptic Plasticity ◽  
Western Blot ◽  
Cell Viability ◽  
Cell Damage ◽  
Neuroblastoma Cell ◽  
Human Neuroblastoma Cell ◽  
Protective Effects ◽  
Astragaloside Iv ◽  
Neuroprotective Effects ◽  
Human Neuroblastoma

The aim of this study was to investigate whether the neuroprotective effects of astragaloside IV (AS-IV) against hydrogen peroxide (H2O2)-induced damage on human neuroblastoma cell line (SH-SY5Y) are associated with synaptic plasticity. The concentration screening of AS-IV and H2O2 on SH-SY5Y cells and the protective effects of AS-IV on SH-SY5Y cells under H2O2 stress were all determined by MTT assay. The expression of postsynaptic density 95 (PSD-95) and growth-associated protein 43 (GAP-43) were measured by western blot (WB) and inmunofluorescence staining assay under the same treatment conditions. According to the MTT results, the concentration of H2O2 at 50 μmol/L for 3 h was used for the cell damage model, and various concentrations of AS-IV (0.1, 0.2, 0.3, and 0.4 μmol/L) were used to affect SH-SY5Y cells. The MTT results showed that pretreatment of SH-SY5Y cells with AS-IV (0.1, 0.2, 0.3, and 0.4 μmol/L) attenuated the damage induced by H2O2 (50 μmol/L, 51.62% cell viability) and increased cell viability to 64.19, 63.48, 65.86, and 65.81%, respectively. Western blot analysis and immunofluorescence staining showed that the protective effects of AS-IV against SH-SY5Y cell damage caused by H2O2 resulted in reduced expression of PSD-95 and increased expression of GAP-43 in comparison with the H2O2 treatment group. The conclusion shows that AS-IV protected SH-SY5Y cells and enhanced their viability under H2O2 stress. AS-IV may facilitate presynaptic and postsynaptic plasticity to exert protective effects against oxidative damage of SH-SY5Y cells.

scholarly journals In vitroscreening of neuroprotective activity of Indian medicinal plantWithania somnifera

2017 ◽  
Vol 6 ◽  
Author(s):  
Manjeet Singh ◽  
Charles Ramassamy
Keyword(s):  
Neuroblastoma Cell ◽  
Amyloid Β ◽  
Acetylcholinesterase Activity ◽  
Neuroprotective Activity ◽  
Great Promise ◽  
Human Neuroblastoma Cell ◽  
Amyloid Β Peptide ◽  
Aβ Peptide ◽  
Neuroprotective Effects ◽  
Human Neuroblastoma

AbstractCanine cognitive dysfunction (CCD) is an age-dependent neurodegenerative condition characterised by changes in decline in learning and memory patterns. The neurodegenerative features of CCD in ageing dogs and cats are similar to human ageing and Alzheimer's disease (AD). Discovering neuroprotective disease-modifying therapies against CCD and AD is a major challenge. Strong evidence supports the role of amyloid β peptide deposition and oxidative stress in the pathophysiology of CCD and AD. In both the human and canine brain, oxidative damage progressively increases with age. Dietary antioxidants from natural sources hold a great promise in halting the progression of CCD and AD.Withania somnifera(WS), an Ayurvedic tonic medicine, also known as ‘Indian ginseng’ orashwagandhahas a long history of use in memory-enhancing therapy but there is a dearth of studies on its neuroprotective effects. The objective of this study was to investigate whetherWSextract can protect against Aβ peptide- and acrolein-induced toxicity. We demonstrated that treatment withWSextract significantly protected the human neuroblastoma cell line SK-N-SH against Aβ peptide and acrolein in various cell survival assays. Furthermore, treatment withWSextract significantly reduced the generation of reactive oxygen species in SK-N-SH cells. Finally, our results showed thatWSextract is also a potent inhibitor of acetylcholinesterase activity. Thus, our initial findings indicate thatWSextract may act as an antioxidant and cholinergic modulator and may have beneficial effects in CCD and AD therapy.

scholarly journals Optimization of 3D bioprinting of human neuroblastoma cells using sodium alginate hydrogel

2019 ◽  
Author(s):  
Jakub Lewicki ◽  
Joost Bergman ◽  
Caoimhe Kerins ◽  
Ola Hermanson
Keyword(s):  
Cell Culture ◽  
Cell Viability ◽  
Sodium Alginate ◽  
Neuroblastoma Cell ◽  
3D Culture ◽  
Fine Tuning ◽  
Human Neuroblastoma Cell ◽  
3D Bioprinting ◽  
Human Neuroblastoma

AbstractThere are many parameters in extrusion-based three-dimensional (3D) bioprinting of different materials that require fine-tuning to obtain the optimal print resolution and cell viability. To standardize this process, methods such as parameter optimization index (POI) have been introduced. The POI aims at pinpointing the optimal printing speed and pressure to achieve the highest accuracy keeping theoretical shear stress low. Here we applied the POI to optimize the process of 3D bioprinting human neuroblastoma cell-laden 2% sodium alginate (SA) hydrogel using freeform reversible embedding of suspended hydrogels (FRESH). Our results demonstrate a notable difference between optimal parameters for printing 2% SA with and without cells in the hydrogel. We also detected a significant influence of long-term cell culture on the printed constructs. This observation suggests that the POI has to be evaluated in the perspective of the final application. When taking these conditions into consideration, we could define a set of parameters that resulted in good quality prints maintaining high neuroblastoma cell viability (83% viable cells) during 7 days of cell culture using 2% SA and FRESH bioprinting. These results can be further used to manufacture neuroblastoma in vitro 3D culture systems to be used for cancer research.

scholarly journals PI3K activation prevents Aβ42-induced synapse loss and favors insoluble amyloid deposits formation

2019 ◽  
Author(s):  
Mercedes Arnés ◽  
Ninovska Romero ◽  
Sergio Casas-Tintó ◽  
Ángel Acebes ◽  
Alberto Ferrús
Keyword(s):  
Neuroblastoma Cell ◽  
Human Neuroblastoma Cell ◽  
Neuroprotective Effects ◽  
Human Neuroblastoma ◽  
Synapse Loss ◽  
Amyloid Deposits ◽  
Pi3k Activation ◽  
Aβ42 Peptide

AbstractAlzheimer’s disease is, to a large extent, a disease of the synapse triggered by the unbalanced amyloidogenic cleavage of the amyloid precursor protein APP. Excess of Aβ42 peptide in particular is considered a hallmark of the disease. Here we drive the expression of the human Aβ42 peptide to assay the neuroprotective effects of PI3K in adult Drosophila melanogaster. We show that the neuronal expression of the human peptide elicits progressive toxicity in the adult. The pathological traits include reduced axonal transport, synapse loss, defective climbing ability and olfactory perception, as well as life-span reduction. The Aβ42-dependent synapse decay does not involve transcriptional changes in the core synaptic protein encoding genes: bruchpilot, liprin and synaptobrevin. All toxicity features, however, are suppressed by the co-expression of PI3K. Moreover, PI3K activation induces a significant increase of 6E10 and Thioflavin-positive amyloid deposits. Mechanistically, we suggest that Aβ42-Ser26 could be a candidate residue for direct or indirect phosphorylation by PI3K. Finally, along with these in vivo experiments we further analyze Aβ42 toxicity and its suppression by PI3K activation in in vitro assays with SH-SY5Y human neuroblastoma cell cultures, where Aβ42 aggregation into large insoluble deposits is reproduced. Taken together, these results uncover a potential novel pharmacological strategy against this disease with PI3K activation as a target.

Design, Synthesis and Evaluation of 8-Thiosubstituted 1,3,7- Trimethylxanthine Hydrazones with In-vitro Neuroprotective and MAO-B Inhibitory Activities

2020 ◽  
Vol 16 (3) ◽  
pp. 326-339 ◽  
Author(s):  
Javor Mitkov ◽  
Alexandra Kasabova-Angelova ◽  
Magdalena Kondeva-Burdina ◽  
Virginia Tzankova ◽  
Diana Tzankova ◽  
...  
Keyword(s):  
Biological Activities ◽  
Neuroblastoma Cell ◽  
Neuroblastoma Cell Line ◽  
Human Neuroblastoma Cell ◽  
Significant Activity ◽  
Neuroprotective Effects ◽  
Human Neuroblastoma ◽  
Mao B ◽  
Chemical Structures

Objective:The syntheses and biological activities of 8-thiosubstituted-1,3,7- trimethylxanthine derivatives bearing an aromatic hydrazide-hydrazone fragment in the side chain at C8 are described.Methods:The chemical structures of the synthesized compounds 6a-m were confirmed based on their MS, FTIR, 1H NMR and 13C NMR analyses.Results:The in vitro investigations of neuroprotective effects manifested on cellular (human neuroblastoma cell line SH-SY5Y) and sub-cellular (isolated rat brain synaptosomes) levels show that compounds 6g and 6i demonstrate statistically significant activity. The performed monoamine oxidase B (MAO-B) inhibition study in vitro show that compounds 6g and 6i possess a significant MAO-B inhibition activity close to L-deprenyl.Conclusion:These results suggest that such compounds may be utilized for the development of new candidate MAO-B inhibitors for the treatment of Parkinson’s disease.

Valproic acid enhances etoposide induced cytotoxicity in neuroblastoma cells

2007 ◽  
Vol 25 (18_suppl) ◽  
pp. 20010-20010
Author(s):  
D. G. Aguilera ◽  
C. Das ◽  
J. Wolff ◽  
P. Zage ◽  
V. Gopalakrishnan
Keyword(s):  
Valproic Acid ◽  
Cell Death ◽  
Cell Viability ◽  
Neuroblastoma Cell ◽  
Neuroblastoma Cells ◽  
Human Neuroblastoma Cell ◽  
Synergistic Activity ◽  
Dependent Manner ◽  
Cell Viability Assay ◽  
Human Neuroblastoma

20010 Background: Metastastic neuroblastoma is resistant to treatment and prolonged response is difficult to achieve therefore new therapies are necessary. Etoposide, a topoisomerase II inhibitor is often used for its treatment. Valproic acid (VPA) has histone deacetylase inhibitor (HDI) activity. Epigenetic alterations described in neuroblastoma tumors make VPA a good candidate to evaluate for potentiation of etoposide-mediated cytotoxicity. We evaluate the effects of VPA in combination with etoposide in neuroblastoma cells. Methods: Human neuroblastoma cell lines SKNAS and SKNSH were incubated with 1.5 mM VPA and increasing concentrations of etoposide from 1x10-6 to 1 mM. Cell viability assay were measured with MTT assays. Results: We observed that VPA and etoposide independently decreased cell viability in a time and concentration dependent manner. The co-incubation with both drugs greatly enhanced the cytotoxicity of etoposide. IC50 for SKNSH cells treated with etoposide were approximately 1x10–3, 1.8x10–4, and 3x10- 5mM at 24, 72 and 96 hours, respectively. With the addition of VPA we found that cell viability was reduced approximately by 10 fold at each time point. At 72 and 96 hours 100 percent cell death was achieved at 0.1 mM of etoposide. IC50 for SKNAS cells treated with etoposide were approximately 1.8x10–3 mM and 6x10–4 mM at 72 and 96 hours, respectively. With the addition of VPA, IC50s were reduced by approximately 5 fold at the same exposure times. Further confirmation of synergistic activity was demonstrated with the use of the fraction product method of Webb formula. Conclusions: Our results demonstrate that VPA potentiates the cytotoxic effects of etoposide on neuroblastoma cells. by altering gene expression and rendering the cells more sensitive to etoposide induced cell death. Finally, since these agents have a proven track record of safety and efficacy in patients with neuroblastoma, this data supports the use of this combination in a phase I trial in patients with neuroblastoma. No significant financial relationships to disclose.

scholarly journals A Galantamine–Curcumin Hybrid Decreases the Cytotoxicity of Amyloid-Beta Peptide on SH-SY5Y Cells

2021 ◽  
Vol 22 (14) ◽  
pp. 7592
Author(s):  
Kirilka Mladenova ◽  
Georgi Stavrakov ◽  
Irena Philipova ◽  
Mariyana Atanasova ◽  
Svetla Petrova ◽  
...  
Keyword(s):  
Amyloid Beta ◽  
Neuroblastoma Cell ◽  
Neuroblastoma Cell Line ◽  
Human Neuroblastoma Cell ◽  
Protective Effects ◽  
Human Neuroblastoma ◽  
Calcium Dysregulation ◽  
Beta Peptide ◽  
Similar Mode ◽  
Α7 Nachrs

Misfolded amyloid beta (Aβ) peptides aggregate and form neurotoxic oligomers. Membrane and mitochondrial damages, calcium dysregulation, oxidative stress, and fibril deposits are among the possible mechanisms of Aβ cytotoxicity. Galantamine (GAL) prevents apoptosis induced by Aβ mainly through the ability to stimulate allosterically the α7 nAChRs and to regulate the calcium cytosolic concentration. Here, we examined the cytoprotective effects of two GAL derivatives, namely compounds 4b and 8, against Aβ cytotoxicity on the human neuroblastoma cell line SH-SY5Y. The protective effects were tested at simultaneous administration, pre-incubation and post-incubation, with Aβ. GAL and curcumin (CU) were used in the study as reference compounds. It was found that 4b protects cells in a similar mode as GAL, while compound 8 and CU potentiate the toxic effects of Aβ. Allosteric stimulation of α7 nAChRs is suggested as a possible mechanism of the cytoprotectivity of 4b. These and previous findings characterize 4b as a prospective non-toxic multi-target agent against neurodegenerative disorders with inhibitory activity on acetylcholinesterase, antioxidant, and cytoprotective properties.

scholarly journals S1P Stimulates Erythropoietin Production in Mouse Renal Interstitial Fibroblasts by S1P1 and S1P3 Receptor Activation and HIF-2α Stabilization

2021 ◽  
Vol 22 (17) ◽  
pp. 9467
Author(s):  
Redona Hafizi ◽  
Faik Imeri ◽  
Roland H. Wenger ◽  
Andrea Huwiler
Keyword(s):  
Cell Line ◽  
Neuroblastoma Cell ◽  
Active Form ◽  
Primary Source ◽  
Fibroblast Cell ◽  
Receptor Activation ◽  
Human Neuroblastoma Cell ◽  
Protective Effects ◽  
Human Neuroblastoma ◽  
S1p Receptor

Erythropoietin (Epo) is the critical hormone for erythropoiesis. In adults, Epo is mainly produced by a subset of interstitial fibroblasts in the kidney, with minor amounts being produced in the liver and the brain. In this study, we used the immortalized renal interstitial fibroblast cell line FAIK F3-5 to investigate the ability of the bioactive sphingolipid sphingosine 1-phosphate (S1P) to stimulate Epo production and to reveal the mechanism involved. Stimulation of cells with exogenous S1P under normoxic conditions (21% O2) led to a dose-dependent increase in Epo mRNA and protein levels and subsequent release of Epo into the medium. S1P also enhanced the stabilization of HIF-2α, a key transcription factor for Epo expression. S1P-stimulated Epo mRNA and protein expression was abolished by HIF-2α mRNA knockdown or by the HIF-2 inhibitor compound 2. Furthermore, the approved S1P receptor modulator FTY720, and its active form FTY720-phosphate, both exerted a similar effect on Epo expression as S1P. The effect of S1P on Epo was antagonized by the selective S1P1 and S1P3 antagonists NIBR-0213 and TY-52156, but not by the S1P2 antagonist JTE-013. Moreover, inhibitors of the classical MAPK/ERK, the p38-MAPK, and inhibitors of protein kinase (PK) C and D all blocked the effect of S1P on Epo expression. Finally, the S1P and FTY720 effects were recapitulated in the Epo-producing human neuroblastoma cell line Kelly, suggesting that S1P receptor-dependent Epo synthesis is of general relevance and not species-specific. In summary, these data suggest that, in renal interstitial fibroblasts, which are the primary source of plasma Epo, S1P1 and 3 receptor activation upregulates Epo under normoxic conditions. This may have a therapeutic impact on disease situations such as chronic kidney disease, where Epo production is impaired, causing anemia, but it may also have therapeutic value as Epo can mediate additional tissue-protective effects in various organs.

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