Neuroprotective Role Of Vitamin Research Articles

Alemtuzumab-Induced Secondary Autoimmune Skin Disorders as Side Effects of Multiple Sclerosis Therapy: Problem That Can Be Influenced or Fate? A Narrative Overview of The Literature A Neuroprotective Role of Vitamin D?

At present, no cure for multiple sclerosis can be made possible with the pharmaceuticals available, nor can a gradual progression of multiple sclerosis be prevented. In the management of multiple sclerosis, it is therefore necessary to determine existing autoimmune diseases through anamnesis before starting alemtuzumab therapy with disease modifying therapy. With previously existing autoimmune diseases or as prophylaxis, comorbidities can be influenced by vitamin D supplementation. Secured pathophysiological and immunological mechanisms of vitamin D on autoimmunological processes support the daily, individually high-dose oral vitamin D intake. This add-on therapy should positively influence the quality of life of persons with multiple sclerosis in the long term. So that the patients do not reject the highly efficient multiple sclerosis therapy for fear of side effects, this therapy offer is a way of avoiding side effects of alemtuzumab administration, such as alopecia, vitiligo, and thyroid diseases, and of decisively influencing the course of MS. This increases the compliance of the persons with multiple sclerosis in therapy. The pathophysiological mechanisms of alopecia and vitiligo are shown. The immunological mechanisms of vitamin D and its influence on autoimmune diseases are described. The previous use of vitamin D in the therapy of these skin diseases is presented and oral supplementation is put up for discussion. The additional neuroprotective effect is evident. Preventing infection with oral vitamin D supplements, particularly in coronavirus disease 2019, may prevent or mitigate multiple sclerosis exacerbations.

Neuroprotective role of vitamin D in primary neuronal cortical culture.

BackgroundA role of Vitamin D in brain development and function has been gaining support over the last decade. There are compelling pieces of evidence that suggest vitamin D may have a neuroprotective role. The administration of vitamin D or its metabolites has been shown to reduce neurological injury and/or neurotoxicity in a variety of animal systems. The detail biochemical mechanism mediating neurons, to its ability to withstand greater oxidative stress in the presence of Vitamin D is unclear. This study was undertaken to study the biochemical effect of treatments of primary cortical neuronal cultures, with the active form of vitamin D(1,25(OH)2D3), against the induced oxidative stress.MethodsPrimary neuronal cultures from cerebral cortex were set up from neonatal (from 6 to 7 days old) Wister Rat's brain. Different doses of [1,25(OH)2D3], ranges from 0 to 1 μg/ml, was added to the culture medium and the cells were cultured in its presence for 24 h to 120 h. The effect of induced extracellular oxidative stress was measured by subjecting these cultured cells with 0.5 mM H2O2 for 2 h, prior to collection of condition medium and the cell pellet for biochemical assay. The control and H2O2 treated cultures were maintained in similar culture conditions, for similar periods of time without any [1,25(OH)2D3] treatments.ResultThe optimum concentration of [1,25(OH)2D3] for treatment of primary cortical neuronal cultures was found to be 0.25 μg/ml by Trypan exclusion assay and MTT assay. Pre-treatments of cultured neuronal cells with 0.25 μg/ml of [1,25(OH)2D3] caused significantly increased levels of reduced glutathione, accompanied by a similar increase in the enzyme levels of GST, to neutralize the induced oxidative stress by H2O2. The level of Lipid peroxidation was significantly higher in the cells treated with H2O2 alone, but it was completely reversed in the neuronal cultures pre-treated with [1,25(OH)2D3]. The levels of Catalase enzyme also significantly reduced (≥0.05) in the [1,25(OH)2D3] pre-treated neuronal cultures.ConclusionWe concluded that the systemic treatment of primary neuronal cultures with [1,25(OH)2D3] gave better protection to neurons against the induced oxidative stress, as shown by quantitative measurements of various biomarkers of oxidative stress. This study also suggested that Vitamin D is vital for the growth, survival, and proliferation of the neurons and hence it has a potential therapeutic role against various neurodegenerative diseases.

Vitamin D3 Reverses the Hippocampal Cytoskeleton Imbalance But Not Memory Deficits Caused by Ovariectomy in Adult Wistar Rats.

The objective of study was to investigate changes caused by ovariectomy (OVX) on aversive and non-aversive memories, as well as on cytoskeleton phosphorylating system and on vitamin D receptor (VDR) immunocontent in hippocampus. The neuroprotective role of vitamin D was also investigated. Ninety-day-old female Wistar rats were divided into four groups: SHAM, OVX, VITAMIN D and OVX+VITAMIN D; 30days after the OVX, vitamin D supplementation (500IU/kg), by gavage, for 30days was started. Results showed that OVX impaired short-term and long-term recognition, and long-term aversive memories. OVX altered hippocampal cytoskeleton phosphorylating system, evidenced by the hyperphosphorylation of glial fibrillary acidic protein (GFAP), low molecular weight neurofilament subunit (NFL), medium molecular weight neurofilament subunit (NFM) and high molecular weight neurofilament subunit (NFH), and increased the immunocontent of c-Jun N-terminal protein kinases (JNK), Ca2+/calmodulin-dependent protein kinase II (PKCaMII) and of the sites phosphorylated lysine-serine-proline (KSP) repeats, Ser55 and Ser57. Vitamin D reversed the effects caused by OVX on cytoskeleton in hippocampus, but it was not able to reverse the effects on memory.

Neuroprotective Role of Vitamin B 3 in Experimentally Induced Oxidative Stress

Paraquat is a widely used herbicide. The main mechanism underlying PQ toxicity is oxidative stress. Niacin (nicotinic acid) a precursor for NAD+ It has also been reported to possess oxygen radical scavenging activity. The enzyme PARP-1 is activated by DNA strand breaks, using NAD+ as a substrate. Thus, the present study aimed to assess the magnitude of oxidative DNA damage and the role of PARP and the advantages of modulating its activity by niacin supplementation in experimentally induced oxidative stress by PQ. 50 male albino rats were equally divided into five groups; the first and second groups were the control and PQ treated groups respectively while the 3rd group was nicotinic acid treated group; the 4th and 5th groups were co- and post treated PQ treated rats with nicotinic acid respectively. Serum 8-hydroxy-2'-deoxyguanosine and brain MDA levels in PQ treated group showed a significant increase when compared with control group, while levels of PARP activity and TAC in PQ treated group showed a significant decrease when compared with control group. A significant increase of PARP activity & TAC and a significant decrease in serum 8-hydroxy-2'-deoxyguanosine&MDA after nicotinic acid injection when compared with control group was observed. Post-treatment with nicotinic acid improved the biochemical and histopathological alterations in brain treated with nicotinic acid, while co-treatment with nicotinic acid protected against ROS production.