folic acid/hypoxia

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Folic acid supplementation repressed hypoxia-induced inflammatory response via ROS and JAK2/STAT3 pathway in human promyelomonocytic cells.

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Hypoxia is associated with inflammation and various chronic diseases. Folic acid is known to ameliorate inflammatory reactions, but the metabolism of folic acid protecting against hypoxia-induced injury is still unclear. In our study, we examined the inflammatory signal transduction pathway in human

Folic Acid Can Contribute to Memory Deficit and Na+, K+- ATPase Failure in the Hippocampus of Adolescent Rats Submitted to Hypoxia- Ischemia.

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Recent findings have demonstrated a dual effect of the folic acid (FA) supplementation on the nervous system of rats. We found that FA treatment prevented memory impairment and Na(+), K(+)- ATPase inhibition in the striatum and cortex in adult rats that suffered neonatal hypoxia-ischemia (HI).

Folic Acid Attenuates Vascular Endothelial Cell Injury Caused by Hypoxia via the Inhibition of ERK1/2/NOX4/ROS Pathway.

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Coronary artery disease is a disease with high morbidity and mortality, in which vascular endothelial dysfunction plays an important role. Hypoxia leads to the inflammation and oxidative stress in endothelial cells, which results in the endothelial injury. The present study was designed to

Hypoxia-responsive folic acid conjugated glycol chitosan nanoparticle for enhanced tumor targeting treatment.

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Hypoxia is a characteristic feature of various ischemic diseases, including cancer. This study describes the development of glycol chitosan nanoparticles, hydrophobically modified with 4-nitrobenzyl chloroformate and folic acid (FA), that can specifically release drugs under hypoxic conditions. This

Folic Acid Represses Hypoxia-Induced Inflammation in THP-1 Cells through Inhibition of the PI3K/Akt/HIF-1α Pathway.

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Though hypoxia has been implicated as a cause of inflammation, the underlying mechanism is not well understood. Folic acid has been shown to provide protection against oxidative stress and inflammation in patients with cardiovascular disease and various models approximating insult to tissue via

Folic Acid Promotes Recycling of Tetrahydrobiopterin and Protects Against Hypoxia-Induced Pulmonary Hypertension by Recoupling Endothelial Nitric Oxide Synthase.

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OBJECTIVE Nitric oxide (NO) derived from endothelial NO synthase (eNOS) has been implicated in the adaptive response to hypoxia. An imbalance between 5,6,7,8-tetrahydrobiopterin (BH4) and 7,8-dihydrobiopterin (BH2) can result in eNOS uncoupling and the generation of superoxide instead of NO.

Folic acid prevents behavioral impairment and Na(+), K(+) -ATPase inhibition caused by neonatal hypoxia-ischemia.

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Folic acid plays an important role in neuroplasticity and acts as a neuroprotective agent, as observed in experimental brain ischemia studies. The aim of this study was to investigate the effects of folic acid on locomotor activity, aversive memory and Na(+),K(+)-ATPase activity in the frontal

Folic acid supplementation during pregnancy prevents cognitive impairments and BDNF imbalance in the hippocampus of the offspring after neonatal hypoxia-ischemia.

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Folic acid (FA) supplementation (400 μg/day) has been recommended during pregnancy to prevent neural tube defects. However, in some countries, flours are required to be fortified with FA, possibly increasing the levels of this vitamin in pregnant women. Our previous studies have evidenced a dual

Gestational folic acid supplementation does not affects the maternal behavior and the early development of rats submitted to neonatal hypoxia-ischemia but the high supplementation impairs the dam's memory and the Na+, K+ - ATPase activity in the pup's hippocampus.

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Folic acid (FA) is a B-complex vitamin important to the development of the fetus, being supplemented during pregnancy. Our recent findings showed that gestation supplementation (normal and excess doses) prevented the cognitive deficits and BDNF imbalance in adult rats that were submitted to neonatal

Peritubular capillary loss after mouse acute nephrotoxicity correlates with down-regulation of vascular endothelial growth factor-A and hypoxia-inducible factor-1 alpha.

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Although the response of kidneys acutely damaged by ischemia or toxins is dominated by epithelial destruction and regeneration, other studies have begun to define abnormalities in the cell biology of the renal microcirculation, especially with regard to peritubular capillaries. We explored the

Folic Acid Exerts Post-Ischemic Neuroprotection In Vitro Through HIF-1α Stabilization.

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The constant failure of single-target drug therapies for ischemic stroke necessitates the development of novel pleiotropic pharmacological treatment approaches, to effectively combat the aftermath of this devastating disorder. The major objective of our study involves a multi-target drug repurposing

A genetic deficiency in folic acid metabolism impairs recovery after ischemic stroke.

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Stroke is a leading cause of disability and death world-wide and nutrition is a modifiable risk factor for stroke. Metheylenetetrahydrofolate reductase (MTHFR) is an enzyme involved in the metabolism of folic acid, a B-vitamin. In humans, a polymorphism in MTHFR (677C→T) is linked to increased risk

Multi-Parametric MRI Detects Longitudinal Evolution of Folic Acid-Induced Nephropathy in Mice.

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The rodent model of folic acid (FA)-induced acute kidney injury (AKI) provides a useful model for studying human AKI, but little is known about longitudinal changes in renal hemodynamics and evolution of renal fibrosis in vivo. In this work, we aimed to longitudinally assess renal structural and

Folic acid attenuates cobalt chloride-induced PGE2 production in HUVECs via the NO/HIF-1alpha/COX-2 pathway.

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Prostaglandin E2 (PGE2), an important lipid inflammatory mediator involved in the progression of vascular diseases, can be induced by hypoxia in many cell types. While folic acid has been shown to protect against inflammation in THP-1 cells during hypoxia and hypoxia-induced endothelial cell injury,

The effect of oxidative stress induced by tert-butylhydroperoxide under distinct folic acid conditions: An in vitro study using cultured human trophoblast-derived cells.

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Preeclampsia is a pregnancy disorder characterized by high maternal blood pressure, fetal growth restriction and intrauterine hypoxia. Folic acid is a vitamin required during pregnancy. In this work, we investigated the relationship between preeclampsia and the intake of distinct doses of folic acid

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