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 Vitamin D, Depressive Symptoms, and Covid-19 Pandemic

2021 ◽  
Vol 15 ◽  
Author(s):  
Gilciane Ceolin ◽  
Giulia Pipolo Rodrigues Mano ◽  
Natália Schmitt Hames ◽  
Luciana da Conceição Antunes ◽  
Elisa Brietzke ◽  
...  
Keyword(s):  
Vitamin D ◽  
Depressive Symptoms ◽  
Vitamin D3 ◽  
Tryptophan Hydroxylase ◽  
Biological Effects ◽  
Active Form ◽  
Sun Exposure ◽  
Monoamine Oxidase A ◽  
Distance Measures ◽  
The Brain

Graphical AbstractRole of vitamin D in the development of depressive symptoms. The synthesis of vitamin D from sunlight is impaired by lockdown and social distance measures imposed by the governments around the world during COVID-10 pandemic. Endogenous vitamin D synthesis initiates in the skin when 7-dehydrocholesterol (7-DHC) is converted in pre-vitamin D3 and then vitamin D3 [25(OH)D3]. It is transported through blood circulation by the vitamin D binding protein (VDBP) to the liver, the kidney, and the brain, where can be converted in its the active form [1,25(OH)2D3]. In the brain, the biological effects of 1,25(OH)2D3 are largely mediated by vitamin D receptor (VDR) through genomic mechanisms, which influence several aspects of serotonin metabolism, such as increasing serotonin synthesis by induction of the tryptophan hydroxylase 2 (TPH2) gene expression; influencing the expression of serotonin reuptake transporter (SERT) and the levels of monoamine oxidase-A (MAO-A), responsible to serotonin catabolism; and indirectly may regulate the synthesis of melatonin that improve the circadian rhythm. This mechanism can be impaired during social isolation and consequent reduction of vitamin D due to low sun exposure during the pandemic, which could contribute to the development of depressive symptoms.

scholarly journals Klotho-Dependent Role of 1,25(OH)2D3 in the Brain

Neurosignals ◽  
2021 ◽  
Vol 29 (1) ◽  
pp. 14-23
Keyword(s):  
Oxidative Stress ◽  
Vitamin D ◽  
Mineral Metabolism ◽  
Biological Activities ◽  
Active Form ◽  
Early Death ◽  
Premature Aging ◽  
Vitamin D Metabolism ◽  
Brain Functions ◽  
The Brain

The antiaging protein Klotho is encoded by the Klotho gene first identified as an 'aging suppressor', in mice. Klotho deficiency is involved in premature aging and early death, while its overexpression is related to longevity. Klotho is mostly expressed in the kidney, but also in the brain, and in other organs. Two forms of Klotho, the cell membrane and secreted form, have pleiotropic activities that include regulation of general metabolism, oxidative stress, and mineral metabolism that correlates with its effect on accelerating aging. Membrane Klotho serves as an obligate co-receptor for the fibroblast growth factor (FGF), while secreted Klotho plays its role as a humoral factor. Klotho protein participates in the regulation of several biological activities, including regulation of calcium-phosphate homeostasis and PTH as well as vitamin D metabolism. The active form of vitamin D, 1,25(OH)2D3 (1,25-dihydroxy-vitamin D3 = calcitriol), acts as a neurosteroid that participates in the regulation of multiple brain functions. It provides neuroprotection and suppresses oxidative stress, inhibits inflammation and inflammatory mediators, and stimulates various neurotrophins. Calcitriol is involved in many brain-related diseases, including multiple sclerosis, Alzheimer´s disease, Parkinson´s disease, and schizophrenia. This review covers the most recent advances in Klotho research and discusses Klotho-dependent roles of calcitriol in neuro-psycho-pathophysiology.

Exploring the Role of Remote Ischemic Preconditioning In Long Term Cognitive Impairment after Global Ischemia-Reperfusion-Induced Vascular Dementia in Mice

2020 ◽  
Author(s):  
Amteshwar Singh Jaggi
Keyword(s):  
Cognitive Impairment ◽  
Cerebral Ischemia ◽  
Vascular Dementia ◽  
Ischemic Preconditioning ◽  
Ischemia Reperfusion ◽  
Remote Ischemic Preconditioning ◽  
Global Cerebral Ischemia ◽  
Cerebral Ischemic ◽  
The Brain

Aim: The aim of the present study is to explore the neuroprotective effects of remote ischemic preconditioning in long term cognitive impairment after global cerebral ischemia induced-vascular dementia in mice. Material and methods: The mice were subjected to global cerebral ischemia by occluding the bilateral common carotid arteries for 12 minutes followed by the 24 hours of the reperfusion. The remote ischemic preconditioning stimulus was delivered in the form of 4 cycles of ischemia/reperfusion for 5 minutes each. The cerebral ischemic injury induced-long term cognitive impairment-related learning and memory alterations was assessed using morris water maze, the motor performances of the animals were evaluated using rota-rod test and neurological severity score. The cerebral infract size of the brain were quantified using triphenyltetrazolium chloride staining. Results: Global cerebral ischemia causes long term memory impairment, decreases motor performances and increases the brain infract size in animals. The delivery of remote ischemic preconditioning stimulus significantly abolished the long-term cognitive impairment and ameliorates the motor performances as well as cerebral infract size in brain. Conclusion: The remote ischemic preconditioning mediates neuro protection against global cerebral ischemic injury induced long-term cognitive impairment.

Ethyl-acetate fraction of Trichilia catigua restores long-term retrograde memory and reduces oxidative stress and inflammation after global cerebral ischemia in rats

2018 ◽  
Vol 337 ◽  
pp. 173-182 ◽  
Author(s):  
Jacqueline Godinho ◽  
Rúbia Maria Weffort de Oliveira ◽  
Anacharis Babeto de Sa-Nakanishi ◽  
Cristiano Correia Bacarin ◽  
Claudia Hitomi Huzita ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cerebral Ischemia ◽  
Ethyl Acetate ◽  
Ethyl Acetate Fraction ◽  
Global Cerebral Ischemia ◽  
Retrograde Memory

scholarly journals Capsaicin exhibits neuroprotective effects in a model of transient global cerebral ischemia in Mongolian gerbils

2005 ◽  
Vol 144 (5) ◽  
pp. 727-735 ◽  
Author(s):  
Simona Pegorini ◽  
Daniela Braida ◽  
Chiara Verzoni ◽  
Chiara Guerini-Rocco ◽  
Gian Giacomo Consalez ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Global Cerebral Ischemia ◽  
Mongolian Gerbils ◽  
Neuroprotective Effects ◽  
Transient Global Cerebral Ischemia

Effect of Propofol and Fentanyl on Brain Oxidative Stress after Systemic Lipopolysaccharide Injection in Rats

2021 ◽  
Vol 11 ◽  
Author(s):  
Omar M.E. Abdel-Salam ◽  
Eman R. Youness ◽  
Nadia A. Mohammed ◽  
Amr M.M. Ibrahim
Keyword(s):  
Oxidative Stress ◽  
Active Form ◽  
Saline Group ◽  
Paraoxonase 1 ◽  
Stress Markers ◽  
Anesthetic Agents ◽  
Systemic Endotoxemia ◽  
Brain Oxidative Stress ◽  
The Brain ◽  
Different Doses

Systemic inflammation causes brain oxidative stress, a prerequisite for neurodegeneration. In this study, we investigated the effect of the anesthetic agents propofol and fentanyl on brain oxidative stress during mild systemic endotoxemia induced by lipopolysaccharide (LPS) endotoxin. For this purpose, rats were administered LPS (400 μg/kg, intraperitoneally; i.p.), treated at the same time with different doses of propofol or fentanyl, i.p., and euthanized 4 h later. Other groups were treated with the saline, only propofol, or only fentanyl. Oxidative stress markers including malondialdehyde (MDA), nitric oxide (NO), and reduced glutathione (GSH) were determined. In addition, nuclear factor kappaB (NF-kB), paraoxonase-1 (PON-1), and butyrylcholinesterase (BChE) activities were measured in the brain tissue. Results showed that compared with the saline group, administration of LPS caused a marked and significant increase in brain MDA and NO combined with depletion of GSH and decreased PON-1 and BChE activities. Additionally, the active form of NF-kB was significantly increased in the brain of LPS only-treated rats. Treatment with propofol or fentanyl led to a marked and significant decrease in the levels of brain MDA and NO together with a significant increase in GSH and restoration of PON-1 and BChE activities. Furthermore, lower levels of active form of NF-kB were found following treatment with propofol or fentanyl compared with those in the LPS only group. Collectively, these results suggest that propofol and fentanyl exhibit an antioxidant action and attenuate the endotoxin-induced brain oxidative stress.

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