Mechanisms of Neuroprotective Action of Vitamin D<sub>3</sub>

Kalueff, Allan V.; Еремин, К. О.; Tuohimaa, Pentti

doi:10.1023/b:biry.0000040196.65686.2f

Cited by 3,665 publications

(85 citation statements)

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“…Cekic et al have found that the activation of the VDR attenuated the inflammatory response induced by TBI [26]. Moreover, Kalueff et al have shown that VDR activation up-regulated free radical scavenging and down-regulated oxidative stress [27]. This pathogenesis ultimately leads to neuronal apoptosis.…”

Section: Discussionmentioning

confidence: 99%

Induction of the Vitamin D Receptor Attenuates Autophagy Dysfunction-Mediated Cell Death Following Traumatic Brain Injury

Chen

Feng

Cui

et al. 2017

Cell Physiol Biochem

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Background/Aims: Traumatic brain injury (TBI) is a major public health problem in the world and causes high rates of mortality and disability. Recent evidence suggests that vitamin D (VD) has neuroprotective actions and can promote function recovery after TBI. In vitro and in vivo studies have demonstrated that autophagy could be enhanced following supplementation with an active metabolite of VD (calcitriol). However, it is unclear whether autophagy participates in the protective effects of calcitriol after TBI. To test this hypothesis, we examined the protective effects of calcitriol on TBI-induced neurological impairment and further investigated whether calcitriol could modulate autophagy dysfunction-mediated cell death in the cortex region of rat brain. Methods: Eighty-five male rats (250-280 g) were randomly assigned to sham (n=15), TBI model (TBI, n=35) and calcitriol treatment (calcitriol, n=35) groups. Rats were injected intraperitoneally with calcitriol (1 µg/kg) at 30 min, 24 h and 48 h post-TBI in the calcitriol group. The lysosomal inhibitor, chloroquine (CQ), was used to evaluate autophagic flux in the TBI and calcitriol groups. Neurological functions were evaluated via the modified neurological severity score test at 1-7 days after TBI or sham operation, and the terminal deoxynucleotidyl transferase-mediated FITC-dUTP nick-end labeling method was used to evaluate the ability of calcitriol to inhibit apoptosis. The expression of VDR, LC3 and p62 proteins was measured by western blot analysis at 1, 3 and 7 days post-injury Results: Calcitriol treatment attenuated mNSS at 2-7 days post-TBI (P < 0.05 versus TBI group). Calcitriol dramatically increased VDR protein expression compared with the untreated counterparts at 1, 3 and 7 days post-TBI (P < 0.05). The rate of apoptotic cells in calcitriol-treated rats was significantly reduced compared to that observed in the TBI group (P < 0.05). The LC3II/LC3I ratio was decreased in the cortex region at 1, 3 and 7 days post-TBI in rats treated with calcitriol (p < 0.05 versus TBI group), and the p62 expression was also attenuated (p < 0.05 versus TBI group). The LC3II/LC3I ratio in the calcitriol group was significantly increased when pretreated with CQ (P < 0.05). Conclusion: Calcitriol treatment activated VDR protein expression and attenuated neurological deficits in this rat TBI model. The protective effects might be associated with the restoration of autophagy flux and the decrease in apoptosis in the cortex region of rat brain.

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Section: Discussionmentioning

confidence: 99%

Induction of the Vitamin D Receptor Attenuates Autophagy Dysfunction-Mediated Cell Death Following Traumatic Brain Injury

Chen

Feng

Cui

et al. 2017

Cell Physiol Biochem

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“…Overall, we expected 1,25 (OH) 2 D, the active form of Vitamin D 3 , to act in a similar fashion as neuroactive steroids (Losel et al 2003) and possibly decrease elevated Ca 2 + concentration (Moghaddam et al 1994;Kalueff et al 2004) and modulate the GABAergic system (Losel et al 2003) in BSD patients. Our findings of improved mood and increased ACC GABA levels at the end of 8 week Vitamin D 3 supplementation support the proposed model.…”

Section: Discussionmentioning

confidence: 99%

“…Vitamin D 3 has been associated with reductions in brain Ca 2 + levels (Kalueff et al 2004). 1,25 (OH) 2 D may modulate GABA A in the brain in a similar fashion to other neuroactive steroids (Losel et al 2003).…”

Section: Introductionmentioning

confidence: 99%

Vitamin D₃Supplemental Treatment for Mania in Youth with Bipolar Spectrum Disorders

Sikoglu

Navarro

Starr

et al. 2015

Journal of Child and Adolescent Psychopharmacology

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Objective: We aimed to determine the effect of an open-label 8 week Vitamin D 3 supplementation on manic symptoms, anterior cingulate cortex (ACC) glutamate, and c-aminobutyric acid (GABA) in youth exhibiting symptoms of mania; that is, patients with bipolar spectrum disorders (BSD). We hypothesized that an 8 week Vitamin D 3 supplementation would improve symptoms of mania, decrease ACC glutamate, and increase ACC GABA in BSD patients. Single time point metabolite levels were also evaluated in typically developing children (TD). Methods: The BSD group included patients not only diagnosed with BD but also those exhibiting bipolar symptomology, including BD not otherwise specified (BD-NOS) and subthreshold mood ratings (Young Mania Rating Scale [YMRS] ‡ 8 and Clinical Global Impressions -Severity [CGI-S] ‡ 3). Inclusion criteria were: male or female participants, 6-17 years old. Sixteen youth with BSD exhibiting manic symptoms and 19 TD were included. BSD patients were asked to a take daily dose (2000 IU) of Vitamin D 3 (for 8 weeks) as a supplement. Neuroimaging data were acquired in both groups at baseline, and also for the BSD group at the end of 8 week Vitamin D 3 supplementation. Results: Baseline ACC GABA/creatine (Cr) was lower in BSD than in TD (F[1,31] = 8.91, p = 0.007). Following an 8 week Vitamin D 3 supplementation, in BSD patients, there was a significant decrease in YMRS scores (t = -3.66, p = 0.002, df = 15) and Children's Depression Rating Scale (CDRS) scores (t = -2.93, p = 0.01, df = 15); and a significant increase in ACC GABA (t = 3.18, p = 0.007, df = 14). Conclusions: Following an 8 week open label trial with Vitamin D 3 , BSD patients exhibited improvement in their mood symptoms in conjunction with their brain neurochemistry.

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“…Vitamin D downregulates interleukin 6 and upregulates anticonvulsant growth factors such as glial cell-derived neurotrophic factor and neurotrophin-3 [4]. The localization of VDR to the plasma membrane caveolae results in the activation of signal transduction pathways.…”

Section: Epilepsy and Vitamin Dmentioning

confidence: 99%

The Role of the Vitamin D in Neurology: Interrelationships Between Headache, Epilepsy and Vitamin D Deficiency

Sönmez¹

2016

JPNC

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Mechanisms of Neuroprotective Action of Vitamin D₃

Cited by 3,665 publications

References 72 publications

Induction of the Vitamin D Receptor Attenuates Autophagy Dysfunction-Mediated Cell Death Following Traumatic Brain Injury

Induction of the Vitamin D Receptor Attenuates Autophagy Dysfunction-Mediated Cell Death Following Traumatic Brain Injury

Vitamin D₃Supplemental Treatment for Mania in Youth with Bipolar Spectrum Disorders

The Role of the Vitamin D in Neurology: Interrelationships Between Headache, Epilepsy and Vitamin D Deficiency

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Mechanisms of Neuroprotective Action of Vitamin D3

Cited by 3,665 publications

References 72 publications

Induction of the Vitamin D Receptor Attenuates Autophagy Dysfunction-Mediated Cell Death Following Traumatic Brain Injury

Induction of the Vitamin D Receptor Attenuates Autophagy Dysfunction-Mediated Cell Death Following Traumatic Brain Injury

Vitamin D3Supplemental Treatment for Mania in Youth with Bipolar Spectrum Disorders

The Role of the Vitamin D in Neurology: Interrelationships Between Headache, Epilepsy and Vitamin D Deficiency

Contact Info

Product

Resources

About

Mechanisms of Neuroprotective Action of Vitamin D₃

Vitamin D₃Supplemental Treatment for Mania in Youth with Bipolar Spectrum Disorders