Effect of vitamin D treatment on VDR expression in primary cerebral cortical cells in induced oxidative stress

2020 ◽  
pp. 1-10
Author(s):  
Ebtesam Alsulami ◽  
Majed Alokail ◽  
Amani Alghamedi ◽  
Abir Alamro ◽  
Samina Haq
Keyword(s):  
Oxidative Stress ◽  
Vitamin D ◽  
Vitamin D3 ◽  
Cultured Cells ◽  
Neuroprotective Effect ◽  
Sandwich Elisa ◽  
Stress Protein ◽  
Neuronal Cultures ◽  
Primary Neuronal Cultures ◽  
Peripheral Tissues

BACKGROUND: In addition to calcium and phosphate homeostasis in peripheral tissues; vitamin D performs a neuroprotection role in the nervous system. The neuroprotective actions of vitamin D include: increasing vitamin D receptor (VDR) expression, control glutathione synthesis and nitric oxide synthase activity and induce neurotrophins such as nerve growth factor (NGF). VDR mediates cellular actions, and biological responses of the vitamin D. OBJECTIVE: To study the effect of VDR and NGF expression levels by vitamin D3 treatment in induced oxidative stress in primary cortical neuronal cultures. METHOD: Primary neuronal cultures were set up from the cortex region of neonatal rat’s brain. They were cultured for up to 72 h in the presence of 0.25μg/ml vitamin D3. These cells were exposed to 0.5 mM H2O2 for two hours before collecting cell pellet and medium for biochemical assays. Control and H2O2 treated cells were cultured in the absence of vitamin D3 treatment. Sandwich ELISA was used to study NGF expression. Western blotting and Immunofluorescence of cultured cells were used to estimate the expression of VDR. RESULTS: Vitamin D3 treatment increased more significantly (P <  0.001) NGF levels with and without induced oxidative stress. Protein expression studies confirmed the positive correlation between VDR expression and vitamin D3 treatment after 72 h in culture. Moreover, pre-treating the cells with vitamin D3 before H2O2 exposure significantly increase (P <  0.05) VDR expression in comparison with the cells exposed to H2O2 alone. CONCLUSION: The neuroprotective effect of vitamin D3 against oxidative stress could be through up-regulating VDR and NGF levels.

scholarly journals Oxidative Stress Induces Dephosphorylation of τ in Rat Brain Primary Neuronal Cultures

2002 ◽  
Vol 68 (4) ◽  
pp. 1590-1597 ◽  
Author(s):  
Daniel R. Davis ◽  
Brian H. Anderton ◽  
Jean-Pierre Brion ◽  
C. Hugh Reynolds ◽  
Diane P. Hanger
Keyword(s):  
Oxidative Stress ◽  
Rat Brain ◽  
Neuronal Cultures ◽  
Primary Neuronal Cultures

scholarly journals Interaction Effects of Vitamin D Receptor Polymorphisms and Vitamin D3 Supplementation on Plasma Oxidative Stress and Apoptotic Biomarkers Among Breast Cancer Survivors (P05-027-19)

2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Elham Kazemin ◽  
Yasaman Jamshidi-naeini ◽  
Mohammad Esmaeil Akbari ◽  
Nariman Moradi ◽  
Safoora Gharibzadeh ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Oxidative Stress ◽  
Vitamin D ◽  
Linear Regression ◽  
Cancer Survivors ◽  
Vitamin D Receptor ◽  
Vitamin D3 ◽  
Multiple Testing ◽  
Breast Cancer Survivors ◽  
Vitamin D3 Supplementation

Abstract Objectives Interactions of human genes and environmental exposures play a crucial role in cancer etiology and prognosis. We investigated whether response to vitamin D3 supplementation in terms of plasma oxidative stress (OS) and apoptotic biomarkers were mediated by the vitamin D receptor (VDR) single-nucleotide polymorphisms (SNPs) among breast cancer survivors. Methods Two hundred and fourteen women who were diagnosed with breast cancer (invasive or in situ) and had completed all treatment regimens received 4000 IU of vitamin D3 daily for 12 weeks. Anthropometric, dietary, sun exposure, physical activity, as well as laboratory assessments including plasma superoxide dismutase (SOD), total antioxidant capacity (TAC), malondialdehyde (MDA), 8-hydroxy-2′-deoxyguanosine (8-OHdG), and Bcl2 were performed at enrolment and post-intervention. VDR genotyping was performed at ApaI, TaqI, FokI, BsmI, and Cdx-2. Linear regression was used to analyze whether the effect of vitamin D3 supplementation on response variables was modulated by the selected VDR SNPs. Results Linear regression analysis adjusted for age, BMI, on-study plasma 25(OH)D changes, and baseline circulating 25(OH)D indicated that the AA genotype of the ApaI on VDR was associated with greater increase and decrease in plasma Bcl2 [0.21, 95% Confidence Interval (CI) (0.03, 0.39)] and MDA [−0.68, 95% CI (−1.35, −0.02)] compared to aa respectively. This association did not remain statistically significant after correction for multiple testing. Overall, we found no statistically significant interaction of the VDR SNPs and inferred haplotypes with the circulating OS and apoptotic biomarkers except for the FokI BsmI ApaIhaplotype and circulating MDA (p-value for global score = 0.02) after multiple testing correction. Conclusions Our findings indicate a weak interaction between the VDR haplotypes and responses of plasma OS and apoptotic biomarkers to vitamin D3 supplementation. However, further assessments of additional genes and biomarkers with longer intervention periods may further explain the complex interplay between genes and nutrients. Funding Sources Cancer Research Center, National Nutrition and Food Technology Research Institute, and the Endocrine Research Center of Shahid Beheshti University of Medical Sciences.

scholarly journals Phosphorylation of p66Shc and forkhead proteins mediates Aβ toxicity

2005 ◽  
Vol 169 (2) ◽  
pp. 331-339 ◽  
Author(s):  
Wanli W. Smith ◽  
Darrell D. Norton ◽  
Myriam Gorospe ◽  
Haibing Jiang ◽  
Shino Nemoto ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Redox Regulation ◽  
Critical Role ◽  
Ectopic Expression ◽  
Amyloid Β ◽  
Dominant Negative ◽  
Neuronal Cultures ◽  
Amyloid Β Peptide ◽  
Dependent Manner ◽  
Primary Neuronal Cultures

Excessive accumulation of amyloid β-peptide (Aβ) plays an early and critical role in synapse and neuronal loss in Alzheimer's Disease (AD). Increased oxidative stress is one of the mechanisms whereby Aβ induces neuronal death. Given the lessened susceptibility to oxidative stress exhibited by mice lacking p66Shc, we investigated the role of p66Shc in Aβ toxicity. Treatment of cells and primary neuronal cultures with Aβ caused apoptotic death and induced p66Shc phosphorylation at Ser36. Ectopic expression of a dominant-negative SEK1 mutant or chemical JNK inhibition reduced Aβ-induced JNK activation and p66Shc phosphorylation (Ser36), suggesting that JNK phosphorylates p66Shc. Aβ induced the phosphorylation and hence inactivation of forkhead transcription factors in a p66Shc-dependent manner. Ectopic expression of p66ShcS36A or antioxidant treatment protected cells against Aβ-induced death and reduced forkhead phosphorylation, suggesting that p66Shc phosphorylation critically influences the redox regulation of forkhead proteins and underlies Aβ toxicity. These findings underscore the potential usefulness of JNK, p66Shc, and forkhead proteins as therapeutic targets for AD.

scholarly journals Efficacy of Mesenchymal Stem Cell and Vitamin D in the Treatment of Diabetes Mellitus Induced in a Rat Model: Pancreatic Tissues

Coatings ◽  
2021 ◽  
Vol 11 (3) ◽  
pp. 317
Author(s):  
Reham Z. Hamza ◽  
Rasha A. Al-Eisa ◽  
Nahla S. El-Shenawy
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Electron Microscopy ◽  
Vitamin D ◽  
Significant Role ◽  
Diabetic Rats ◽  
Male Rats ◽  
Cytokine Gene Expression ◽  
Histological Structure ◽  
Peripheral Tissues

Treatment with mesenchyme stem cells (MSCs) plays a significant role in the therapies of many diseases such as diabetics. Vitamin D plays a significant role in the development of insulin and can increase the insulin action sensitivity of peripheral tissues. Moreover, there is limited research concerning the mechanism of the therapeutic action of MSCs with the combination of vitamin D (vit. D). Therefore, we evaluated the effect of MSC intervention in a diabetic animal model. Diabetes was induced by streptozotocin (STZ) injection at a dose of 50 mg/kg in adult male rats The diabetic rats were injected with MSCs derived from bone marrow (2 × 106 per rat), either alone or in combination with vit. D through the tail vein for four weeks. Serum insulin, glucose, C-peptide, glycosylated hemoglobin, and lipid profile levels were determined. Pancreatic oxidative stress, histology, and electron microscopy were evaluated, and the gene expression of cytokines was assessed by real-time polymerase chain reaction PCR. MSC treatment suppressed pancreatic inflammatory cytokine secretion and oxidative stress in diabetic rats, resulting in improved pancreatic histology and cellular structure, and the complication of hyperglycemia was observed. Engrafted MSCs were found inside degraded pancreatic regions and regulated inflammatory cytokines. Our results demonstrated that treatment with MSCs and vit. D in combination prevented pancreatic injury via antioxidant and immune regulation in diabetic rats, contributing to the prevention of pancreatic dysfunction, improvement of lipid metabolism, and regulation of cytokine gene expression compared with each one separately. All these mechanisms also improved the histological structure of the pancreas based on transmission electron microscopy. The combination of MSCs and vit. D appears to have contributed to a greater improvement in the diabetic pancreatic complication of rats than was observed by each one separately. Therefore, this association can be used as antidiabetic therapy.

Neuroprotective effect of weak static magnetic fields in primary neuronal cultures

Neuroscience ◽  
2014 ◽  
Vol 278 ◽  
pp. 313-326 ◽  
Author(s):  
M. Ben Yakir-Blumkin ◽  
Y. Loboda ◽  
L. Schächter ◽  
J.P.M. Finberg
Keyword(s):  
Magnetic Fields ◽  
Neuroprotective Effect ◽  
Neuronal Cultures ◽  
Primary Neuronal Cultures ◽  
Static Magnetic Fields

Effect of vitamin D3 supplementation and influence of BsmI polymorphism of the VDR gene of the inflammatory profile and oxidative stress in elderly women with vitamin D insufficiency

2015 ◽  
Vol 66 ◽  
pp. 10-16 ◽  
Author(s):  
Isa Gabriela de Medeiros Cavalcante ◽  
Alexandre Sérgio Silva ◽  
Maria José Carvalho Costa ◽  
Darlene Camati Persuhn ◽  
ChariraTahaMad Ibraim Issa ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Vitamin D ◽  
Vitamin D3 ◽  
Elderly Women ◽  
Vitamin D Insufficiency ◽  
Vdr Gene ◽  
Bsmi Polymorphism ◽  
Vitamin D3 Supplementation ◽  
Inflammatory Profile ◽  
And Oxidative Stress

scholarly journals High-dose Propofol Triggers Short-term Neuroprotection and Long-term Neurodegeneration in Primary Neuronal Cultures from Rat Embryos

2009 ◽  
Vol 37 (3) ◽  
pp. 680-688 ◽  
Author(s):  
M Berns ◽  
L Seeberg ◽  
M Schmidt ◽  
T Kerner
Keyword(s):  
Cell Viability ◽  
Cortical Neurons ◽  
Neuroprotective Effect ◽  
Wistar Rat ◽  
Neuronal Cultures ◽  
High Dose ◽  
Receptor Antagonists ◽  
Primary Neuronal Cultures ◽  
Rat Embryos ◽  
High Doses

This study investigated the effects of propofol on primary neuronal cultures from rat embryos. Primary cortical neuronal cultures were prepared from Wistar rat embryos (E18). The viability of cells exposed to 0.01, 0.1 or 1 mg/ml propofol for up to 48 h was assessed using a methyltetrazolium assay. In order to evaluate the role of γ-aminobutyric acid-A (GABAA) receptors, cells were also pre-incubated with the GABAA-receptor antagonists, gabazine and picrotoxin. Propofol at a concentration of 1 mg/ml significantly reduced cell viability after 12 h. In contrast, this concentration led to a significant increase in cell viability at 3 and 6 h. The GABAA-receptor antagonists did not influence the neurodegenerative effect of propofol but abolished its neuroprotective effect. DNA fragmentation as a marker of apoptosis was elevated after 24 h propofol treatment. These results confirm that high doses of propofol can cause GABAA-receptor triggered neuroprotection and a subsequent time-dependent, but GABAA-independent, neurodegeneration in primary cortical neurons.

scholarly journals Effects of Vitamin D3 on the NADPH Oxidase and Matrix Metalloproteinase 9 in an Animal Model of Global Cerebral Ischemia

2018 ◽  
Vol 2018 ◽  
pp. 1-14 ◽  
Author(s):  
Milica Velimirović ◽  
Gordana Jevtić Dožudić ◽  
Vesna Selaković ◽  
Tihomir Stojković ◽  
Nela Puškaš ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Vitamin D ◽  
Cerebral Ischemia ◽  
Nadph Oxidase ◽  
Vitamin D3 ◽  
Active Form ◽  
Global Cerebral Ischemia ◽  
Mongolian Gerbils ◽  
Stress Changes ◽  
The Brain

Decreased blood flow in the brain leads to a rapid increase in reactive oxygen species (ROS). NADPH oxidase (NOX) is an enzyme family that has the physiological function to produce ROS. NOX2 and NOX4 overexpression is associated with aggravated ischemic injury, while NOX2/4-deficient mice had reduced stroke size. Dysregulation of matrix metalloproteinases (MMPs) contributes to tissue damage. The active form of vitamin D3 expresses neuroprotective, immunomodulatory, and anti-inflammatory effects in the CNS. The present study examines the effects of the vitamin D3 pretreatment on the oxidative stress parameters and the expression of NOX subunits, MMP9, microglial marker Iba1, and vitamin D receptor (VDR), in the cortex and hippocampus of Mongolian gerbils subjected to ten minutes of global cerebral ischemia, followed by 24 hours of reperfusion. The ischemia/reperfusion procedure has induced oxidative stress, changes in the expression of NOX2 subunits and MMP9 in the brain, and increased MMP9 activity in the serum of experimental animals. Pretreatment with vitamin D3 was especially effective on NOX2 subunits, MMP9, and the level of malondialdehyde and superoxide anion. These results outline the significance of the NOX and MMP9 investigation in brain ischemia and the importance of adequate vitamin D supplementation in ameliorating the injury caused by I/R.

scholarly journals Proposed Neuroimmune Roles of Dimethyl Fumarate, Bupropion, S-Adenosylmethionine, and Vitamin D3 in Affording a Chronically Ill Patient Sustained Relief from Inflammation and Major Depression

2020 ◽  
Vol 10 (9) ◽  
pp. 600 ◽  
Author(s):  
Navzer D. Sachinvala ◽  
Naozumi Teramoto ◽  
Angeline Stergiou
Keyword(s):  
Oxidative Stress ◽  
Major Depression ◽  
Vitamin D3 ◽  
Sphenoid Sinus ◽  
Vision Loss ◽  
Chronically Ill ◽  
Dimethyl Fumarate ◽  
Peripheral Tissues ◽  
Physical Exercises ◽  
Literature Searches

We had discussed earlier that, after most of the primary author’s multiple sclerosis (MS) symptoms were lessened by prior neuroimmune therapies, use of dimethyl fumarate (DMF) gradually subdued his asthma and urticaria symptoms, as well as his MS-related intercostal cramping; and bupropion supplemented with S-adenosylmethionine (SAMe) and vitamin D3 (vit-D3) helped remit major depression (MD). Furthermore, the same cocktail (bupropion plus supplements), along with previously discussed routines (yoga, meditation, physical exercises, and timely use of medications for other illnesses), continued to subdue MD during new difficulties with craniopharyngioma, which caused bitemporal vision loss; sphenoid sinus infections, which caused cranial nerve-VI (CN6) palsy and diplopia; and through their treatments. Impressed with the benefit the four compounds provided, in this manuscript, we focus on explaining current neuroimmune literature proposals on how: (1) DMF impedes inflammation, oxidative stress, and cell death in CNS and peripheral tissues; (2) Bupropion curbs anxiety, MD, and enhances alertness, libido, and moods; (3) SAMe silences oxidative stress and depression by multiple mechanisms; and (4) Vit-D3 helps brain development and functioning and subdues inflammation. We realize that herein we have reviewed proposed mechanisms of remedies we discovered by literature searches and physician assisted auto-experimentation; and our methods might not work with other patients. We present our experiences so readers are heartened to reflect upon their own observations in peer-reviewed forums and make available a wide body of information for the chronically ill and their physicians to benefit from.

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