scholarly journals Protective effects of 1α,25-Dihydroxyvitamin D3 on cultured neural cells exposed to catalytic iron

2016 ◽  
Vol 4 (11) ◽  
pp. e12769 ◽  
Author(s):  
Francesca Uberti ◽  
Vera Morsanuto ◽  
Claudio Bardelli ◽  
Claudio Molinari
Keyword(s):  
Neural Cells ◽  
Protective Effects ◽  
Dihydroxyvitamin D3

Estrogens and progestins: molecular effects on brain cells

2010 ◽  
Vol 4 (3) ◽  
Author(s):  
Paolo Mannella ◽  
Tommaso Simoncini ◽  
Andrea Riccardo Genazzani
Keyword(s):  
Sex Steroids ◽  
Molecular Mechanisms ◽  
Neural Cells ◽  
Protective Effects ◽  
Complete Knowledge ◽  
Molecular Effects ◽  
In Vivo Effects ◽  
The Brain

AbstractSex steroids are known to regulate brain function and their role is so important that several diseases are strictly correlated with the onset of menopause when estrogen-progesterone deficiency makes neural cells much more vulnerable to toxic stimuli. Although in the past years several scientists have focused their studies on in vitro and in vivo effects of sex steroids on the brain, we are still far from complete knowledge. Indeed, contrasting results from large clinical trials have made the entire issue much more complicated. Currently we know that protective effects exerted by sex steroids depend on several factors among which the dose, the health of the cells and the type of molecule being used. In this review, we present an overview of the direct and indirect effects of estrogen and progesterone on the brain with specific focus on the molecular mechanisms by which these molecules act on neural cells.

scholarly journals Thrombopoietin Has Protective Effect in Neonatal Hypoxia-Ischemia Rat Model

Blood ◽  
2019 ◽  
Vol 134 (Supplement_1) ◽  
pp. 4898-4898
Author(s):  
Liang Li ◽  
Liuming Yang ◽  
Hongwu Xin ◽  
Beng H Chong ◽  
Mo Yang
Keyword(s):  
Membrane Potential ◽  
Protective Effect ◽  
Brain Damage ◽  
Mitochondrial Membrane Potential ◽  
Rat Model ◽  
Mitochondrial Membrane ◽  
Conflicts Of Interest ◽  
Neonatal Rat ◽  
Neural Cells ◽  
Protective Effects

Thrombopoietin (TPO) is a growth factor for the megakaryocytic lineage. The expression of TPO and TPO receptor (c-mpl) in the central nervous system (CNS) and the role of TPO in neural cells and brain damage models were investigated. Our results showed the expression of TPO in human cerebral hemisphere, cerebellum, cerebrospinal fluid and blood plasma. We found that TPO had a protective effect in hypoxic-ischemic rat model, as indicated by the increased ipsilateral brain weight and neuron density in a neonatal rat model of hypoxic-ischemic brain damage. Recoveries of sensorimotor functions and histopathology were observed in these animals that received TPO. In addition, TPO could promote C17.2 cells proliferation by activating PI3K/Akt signaling pathway, and the proliferation could be reduced to nearly basal level by the pre-treatment with LY 294002. The phosphorylation of AKT, which is a hallmark of activation of each molecule was significantly enhanced after the treatment with TPO in the cells, peaking at 30 min after stimulation with TPO. TPO was also found to have an anti-apoptotic effect which mediated via Bcl-2/BAX and suppressing the mitochondrial membrane potential. Results showed the increased level of Bcl-2 and decreased level of BAX were in the time-dependence manner (0, 5, 15, 30 and 60 mins) in these cells. In addition, the mitochondrial membrane potential was significantly decreased by adding 100 ng/ml TPO. Our results indicated that TPO have neural protective effects. Disclosures No relevant conflicts of interest to declare.

Similar protective effects of BQ-123 and erythropoietin on survival of neural cells and generation of neurons upon hypoxic injury

2005 ◽  
Vol 84 (11) ◽  
pp. 907-913 ◽  
Author(s):  
Lusine Danielyan ◽  
Lars Mueller ◽  
Barbara Proksch ◽  
Daniela Kabisch ◽  
Michael Weller ◽  
...  
Keyword(s):  
Neural Cells ◽  
Protective Effects ◽  
Hypoxic Injury

scholarly journals Protective Effects of Tao-Hong-Si-Wu Decoction on Memory Impairment and Hippocampal Damage in Animal Model of Vascular Dementia

2015 ◽  
Vol 2015 ◽  
pp. 1-12 ◽  
Author(s):  
Lan Han ◽  
Zhaojie Ji ◽  
Weidong Chen ◽  
Dengke Yin ◽  
Fan Xu ◽  
...  
Keyword(s):  
Vascular Dementia ◽  
Memory Impairment ◽  
B Cell Lymphoma ◽  
Artery Occlusion ◽  
Hippocampal Damage ◽  
Neural Cells ◽  
Protective Effects ◽  
Thrombotic Diseases ◽  
Endothelial Growth Factor ◽  
Cerebral Artery Occlusion

Tao-Hong-Si-Wu decoction (TSD) as a traditional chinese medicine (TCM) has been developed to treat thrombotic diseases for hundreds of years, and vascular dementia (VD) is a cognitive dysfunction syndrome caused by cerebral embolism. In this study, the protective effect of TSD on memory impairment and brain damage in rat model of VD induced by middle cerebral artery occlusion (MCAO) was investigated. The study showed that rats in MCAO treatment with TSD for 14 days significantly improved behavioral function, increased densities of neuron, and induced angiogenesis in the brain compared with model rats. TSD also adjusted the neurotransmitter levels, reduced the content of endothelin-1 (ET-1), and induced the activities of vascular endothelial growth factor (VEGF) in hippocampus. Moreover, the immunohistochemical staining and western blotting results also revealed that TSD decreased apoptosis via upregulated B-cell lymphoma-2 (Bcl-2)/Bcl-2 associated X protein (Bax) ratio. These results demonstrated TSD possesses neuroprotective and antidementia properties by preventing the loss of neural cells, adjusting brain neurotransmitter, promoting cerebral blood circulation, and decreasing apoptosis. These results suggested that TSD might be developed as an effective drug for the prevention of VD.

scholarly journals Protective Effects of CISD2 and Influence of Curcumin on CISD2 Expression in Aged Animals and Inflammatory Cell Model

Nutrients ◽  
2019 ◽  
Vol 11 (3) ◽  
pp. 700 ◽  
Author(s):  
Chai-Ching Lin ◽  
Tien-Huang Chiang ◽  
Yu-Yo Sun ◽  
Muh-Shi Lin
Keyword(s):  
Spinal Cord ◽  
Mitochondrial Dysfunction ◽  
Cell Model ◽  
Neural Cells ◽  
Protective Effects ◽  
Curcumin Treatment ◽  
Cord Injury

Background: Inflammation and mitochondrial dysfunction have been linked to trauma, neurodegeneration, and aging. Impairment of CISD2 expression may trigger the aforementioned pathological conditions in neural cells. We previously reported that curcumin attenuates the downregulation of CISD2 in animal models of spinal cord injury and lipopolysaccharide (LPS)-treated neuronal cells. In this study, we investigate (1) the role of CISD2 and (2) how curcumin regulates CISD2 in the aging process. Materials and methods: The serial expression of CISD2 and the efficacy of curcumin treatment were evaluated in old (104 weeks) mice and long-term cultures of neural cells (35 days in vitro, DIV). LPS-challenged neural cells (with or without siCISD2 transfection) were used to verify the role of curcumin on CISD2 underlying mitochondrial dysfunction. Results: In the brain and spinal cord of mice aged P2, 8, 25, and 104 weeks, we observed a significant decrease in CISD2 expression with age. Curcumin treatment in vivo and in vitro was shown to upregulate CISD2 expression; attenuate inflammatory response in neural cells. Moreover, curcumin treatment elevated CISD2 expression levels and prevented mitochondrial dysfunction in LPS-challenged neural cells. The beneficial effects of curcumin in either non-stressed or LPS-challenged cells that underwent siCISD2 transfection were significantly lower than in respective groups of cells that underwent scrambled siRNA-transfection. Conclusions: We hypothesize that the protective effects of curcumin treatment in reducing cellular inflammation associated trauma, degenerative, and aging processes can be partially attributed to elevated CISD2 expression. We observed a reduction in the protective effects of curcumin against injury-induced inflammation and mitochondrial dysfunction in cells where CISD2 expression was reduced by siCISD2.

scholarly journals 1α,25-Dihydroxyvitamin D3 up-regulates IL-34 expression in SH-SY5Y neural cells

2017 ◽  
Vol 23 (7) ◽  
pp. 584-591 ◽  
Author(s):  
Dong Zhang ◽  
Miaomiao Li ◽  
Yang Dong ◽  
Xinhui Zhang ◽  
Xingyun Liu ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Vitamin D ◽  
Core Promoter ◽  
Active Form ◽  
Vitamin D Supplementation ◽  
Neural Cells ◽  
Dependent Manner ◽  
Dihydroxyvitamin D3 ◽  
Protective Function

Vitamin D supplementation is regarded as a novel approach to treat Alzheimer’s disease, but the underlying mechanism remains elusive. The cytokine IL-34 provides strong neuroprotective and survival signals in brain injury and neurodegeneration and could be an immunological mediator for the vitamin D-induced protection. The aim of this study was to investigate whether human IL-34 is up-regulated in neuronal cells by the hormonally active form of vitamin D, 1α,25-dihydroxyvitamin D3 [1α,25(OH)2D3]. We found that IL-34 was detectable in a variety of cell lines and its expression was strongly induced in SH-SY5Y neural cells in a dose- and time-dependent manner by 1α,25(OH)2D3 through the vitamin D receptor (VDR). Furthermore, we identified the core promoter of IL-34 gene and a VDR binding site (CGCCCT) that was required for 1α,25(OH)2D3-induced IL-34 expression. These findings suggest that the induction of IL-34 expression by 1α,25(OH)2D3 may constitute a mechanism that explains the protective function of vitamin D in Alzheimer’s disease.

Isoform-Dependent Effects of Apolipoprotein E on Sphingolipid Metabolism in Neural Cells

2021 ◽  
pp. 1-16
Author(s):  
Makoto Kurano ◽  
Kazuhisa Tsukamoto ◽  
Eri Sakai ◽  
Masumi Hara ◽  
Yutaka Yatomi
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Apolipoprotein E ◽  
Sphingolipid Metabolism ◽  
Neural Cells ◽  
Protective Effects ◽  
Apoe Isoforms ◽  
Potential Association ◽  
Sphingosine 1 Phosphate ◽  
U251 Cells

Background: Sphingosine 1-phosphate (S1P) and ceramides have been implicated in the development of Alzheimer’s disease. Apolipoprotein E (ApoE) isoforms are also involved in the development of Alzheimer’s disease. Objective: We aimed at elucidating the potential association of the ApoE isoforms with sphingolipid metabolism in the central nervous system. Methods: We investigated the modulations of apolipoprotein M (apoM), a carrier of S1P, S1P, and ceramides in Apoeshl mice, which spontaneously lack apoE, and U251 cells and SH-SY5Y cells infected with adenovirus vectors encoding for apoE2, apoE3, and apoE4. Results: In the brains of Apoeshl mice, the levels of apoM were lower, while those of ceramides were higher. In U251 cells, cellular apoM and S1P levels were the highest in the cells overexpressing apoE2 among the apoE isoforms. The cellular and medium contents of ceramides decreased in the order of the cells overexpressing apoE3 > apoE2 and increased in the cells overexpressing apoE4. In SH-SY5Y cells, apoM mRNA and medium S1P levels were also the highest in the cells overexpressing apoE2. The cellular contents of ceramides decreased in the order of the cells overexpressing apoE3 > apoE2 = apoE4 and those in medium decreased in the order of the cells overexpressing apoE3 > apoE2, while increased in the cells overexpressing apoE4. Conclusion: The modulation of apoM and S1P might partly explain the protective effects of apoE2 against Alzheimer’s disease, and the modulation of ceramides might be one of the mechanisms explaining the association of apoE4 with the development of Alzheimer’s disease.

A Quantitative Proteomic Analysis to Reveal Effects of N-acetylcysteine on H2O2-induced Cytotoxicity

2020 ◽  
Vol 17 ◽  
Author(s):  
Jong-Moon Park ◽  
Van-An Duong ◽  
Jeong-Hun Mok ◽  
Doo-Jin Choi ◽  
Hookeun Lee
Keyword(s):  
Lactate Dehydrogenase ◽  
Proteomic Analysis ◽  
Treated Group ◽  
Differentially Expressed ◽  
Neural Cells ◽  
Protective Effects ◽  
Differentially Expressed Proteins ◽  
Protein Protein Interaction ◽  
Data Independent Acquisition ◽  
Liquid Chromatography Tandem Mass

Aims: This study aimed to perform a quantitative analysis of the proteomic changes in neural cells under H2O2 exposure and N-acetylcysteine (NAC) treatment. Objective: This study aimed to identify differentially expressed proteins among control, H2O2-treated group, and NAC+H2O2-treated group as well as reveal proteins involving in the protection of neural cells from H2O2-induced toxicity. Methods: SK-N-MC cell was untreated (control), treated with H2O2 (disease group), pretreated with NAC and then treated with H2O2 (NAC group). Proteins were digested to peptides and analyzed using liquid chromatography-tandem mass spectrometry with the data-independent acquisition. Skyline was used to quantify peptides and proteins. MSstats was used for statistical analysis. Gene ontology and protein-protein interaction were performed using the differentially expressed proteins (DEPs). Results: Cytoprotective effects of NAC on the cell against H2O2-induced toxicity were first proven using a cell viability study and lactate dehydrogenase assay. The proteomic analysis found 93 DEPs in three comparisons. Among them, 37 proteins were differentially expressed under H2O2 exposure. Only 10 DEPs were rescued in the case of NAC pretreatment. Aspartate aminotransferase and L-lactate dehydrogenase B chain were two DEPs involved in the cysteine and methionine metabolism pathway, which might relate to the mechanisms of NAC protective effects. Conclusion: The findings of cell studies and proteomic analysis were in agreement with previous results, confirming the cytoprotective effects of NAC on neural cells against oxidative stress.

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