Vitamin B-Complex Initiates Growth and Development of Human Embryonic Brain Cells In Vitro

Danielyan, Kristine Edgar; Abramyan, R. A.; Galoyan, A. A.; Kevorkian, G. A.

doi:10.1007/s10517-011-1387-8

Cited by 2 publications

(2 citation statements)

References 10 publications

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“…Vitamin B 6 plays a role in certain gene expressions and neurotransmitter synthesis (serotonin, epinephrine, norepinephrine, and gamma-Aminobutyric acid). While, folate is a major requirement for brain and spinal cord development as well as regulation of gene expressions specifically by silencing certain sequences, riboflavin also plays a role in brain development [63–65]. …”

Section: Discussionmentioning

confidence: 99%

Dietary intake, nutrition, and fetal alcohol spectrum disorders in the Western Cape Province of South Africa

May

Hamrick²,

Corbin

et al. 2014

Reproductive Toxicology

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In this study, we describe the nutritional status of women from a South African community with very high rates of fetal alcohol spectrum disorders (FASD). Nutrient intake (24-hours recall) of mothers of children with FASD was compared to mothers of normal controls. Nutrient adequacy was assessed using Dietary Reference Intakes (DRIs). More than 50 percent of all mothers were below the Estimated Average Requirement (EAR) for vitamins A, D, E, and C, thiamin, riboflavin, vitamin B6, folate, calcium, magnesium, iron, and zinc. Mean intakes were below the Adequate Intake (AI) for vitamin K, potassium, and choline. Mothers of children with FASD reported significantly lower intake of calcium, docosapentaenoic acid (DPA), riboflavin, and choline than controls. Lower intake of multiple key nutrients correlates significantly with heavy drinking. Poor diet quality and multiple nutritional inadequacies coupled with prenatal alcohol exposure may increase the risk for FASD in this population.

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Section: Discussionmentioning

confidence: 99%

Dietary intake, nutrition, and fetal alcohol spectrum disorders in the Western Cape Province of South Africa

May

Hamrick²,

Corbin

et al. 2014

Reproductive Toxicology

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“…It is well known that vitamin B is a class of significant nutrient that highly benefit neurological system, and vitamin B complex in low-doses promote the development, maturation, and enlargement of human embryonic brain cells [26]. Actually, vitamin B complex deficiency has been noted in children with cerebral palsy [27], and the effects of vitamin B1 and B12 on facilitating the regeneration of the peripheral have been previously confirmed [28].…”

Section: Discussionmentioning

confidence: 99%

Vitamin B1 and B12 mitigates neuron apoptosis in cerebral palsy by augmenting BDNF expression through MALAT1/miR-1 axis

Zhao

Jian

et al. 2019

Cell Cycle

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Through the roles of vitamin B1 and B12 in neuroprotection and in improving cerebral palsy symptoms have been previously noticed, the action mechanism is still unclear. This study aims to investigate the protective effect of vitamin B1 and B12 on neuron injury in cerebral palsy and to clarify the mechanism of vitamin B1 and B12 inhibiting neurons apoptosis, and to focus on the role of lncRNA MALAT1 in this process. In order to investigate the effect of vitamin B1 and B12 on neurons injury in vivo and on neuron apoptosis in vitro, we, respectively, introduced vitamin B1 and B12 into cerebral palsy rat and in apoptosis-induced N2A neurons by Oxygen Glucose Deprivation/reoxygenation (OGD/R). Our results demonstrated that vitamin B1 and B12 treatment improved the motor and memory functions and ameliorated the neurons injury in cerebral palsy rats. OGD/R treatment repressed the expression of MALAT1 and BDNF and the phosphorylation of PI3K and Akt, and enhanced the miR-1 expression, which were all reversed by vitamin B1 and B12 treatment in N2A neurons. Vitamin B1 and B12 inhibited miR-1 expression through MALAT1, promoted BDNF expression and activated PI3K/Akt signaling through the MALAT1/miR-1 axis. Vitamin B1 and B12 suppressed neuron apoptosis by up-regulating BDNF via MALAT1/miR-1 pathway. MALAT1 interference abolished the neuroprotective effect of vitamin B1 and B12 in cerebral palsy rats. Collectively, vitamin B1 and B12 up-regulates BDNF and its downstream PI3K/ Akt signaling through MALAT1/miR-1 axis, thus suppressing neuron apoptosis and mitigating nerve injury in cerebral palsy rats.

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Vitamin B-Complex Initiates Growth and Development of Human Embryonic Brain Cells In Vitro

Cited by 2 publications

References 10 publications

Dietary intake, nutrition, and fetal alcohol spectrum disorders in the Western Cape Province of South Africa

Dietary intake, nutrition, and fetal alcohol spectrum disorders in the Western Cape Province of South Africa

Vitamin B1 and B12 mitigates neuron apoptosis in cerebral palsy by augmenting BDNF expression through MALAT1/miR-1 axis

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