Nitric oxide: from the mechanism of action to pharmacological effects in cerebrovascular diseases

Fateeva, V V; Vorobyova, O. V.

doi:10.17116/jnevro2017117101131-135

Cited by 8 publications

(1 citation statement)

References 31 publications

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“…Endothelial dysfunction has been identified as one of the most important pathogenetic causes of human cerebrovascular disease (CVD) (1,2). Endothelial dysfunction can cause damage to the blood-brain barrier and can result in a range of neurological disorders, including multiple sclerosis, vascular dementia and subsequent complications of the extremities (3–5).…”

Section: Introductionmentioning

confidence: 99%

Astaxanthin inhibits homocysteine‑induced endothelial cell dysfunction via the regulation of the reactive oxygen species‑dependent VEGF‑VEGFR2‑FAK signaling pathway

et al. 2019

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Increased plasma levels of homocysteine (Hcy) can cause severe damage to vascular endothelial cells. Hcy-induced endothelial cell dysfunction contributes to the occurrence and development of human cerebrovascular diseases (CVDs). Our previous studies have revealed that astaxanthin (ATX) exhibits novel cardioprotective activity against Hcy-induced cardiotoxicity in vitro and in vivo . However, the protective effect and mechanism of ATX against Hcy-induced endothelial cell dysfunction requires further investigation. In the present study, treatment of human umbilical vascular endothelial cells (HUVECs) with Hcy inhibited the migration, invasive and tube formation potentials of these cells in a dose-dependent manner. Hcy treatment further induced a time-dependent increase in the production of reactive oxygen species (ROS), and downregulated the expression of vascular endothelial growth factor (VEGF), phosphorylated (p)-Tyr-VEGF receptor 2 (VEGFR2) and p-Tyr397-focal adhesion kinase (FAK). On the contrary, ATX pre-treatment significantly inhibited Hcy-induced cytotoxicity and increased HUVEC migration, invasion and tube formation following Hcy treatment. The mechanism of action may involve the effective inhibition of Hcy-induced ROS generation and the recovery of FAK phosphorylation. Collectively, our findings suggested that ATX could inhibit Hcy-induced endothelial dysfunction by suppressing Hcy-induced activation of the VEGF-VEGFR2-FAK signaling axis, which indicates the novel therapeutic potential of ATX in treating Hcy-mediated CVD.

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Section: Introductionmentioning

confidence: 99%

Astaxanthin inhibits homocysteine‑induced endothelial cell dysfunction via the regulation of the reactive oxygen species‑dependent VEGF‑VEGFR2‑FAK signaling pathway

et al. 2019

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Involvement of Inducible Nitric Oxide Synthase in Pial Arterial Tone Formation under Metabolic Disorders and Streptozotocin-Induced Diabetes in Rats Kept on a High-Fat Diet

Sokolova

2022

J Evol Biochem Phys

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The use of inhaled nitric oxide (Tianox device) in patients with moderate cognitive impairment

Starchina,

Grishina,

Sokolov

et al. 2023

RJTAO

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Mild cognitive impairment (MCI) is an intermediate stage between normal cognitive function (CF) and dementia. In the general population of elderly, it is diagnosed in 10–15% of cases; in patients attending outpatient appointments, the frequency of diagnosis is 70%. In our country, there is positive experience with the inhalation of nitric oxide, using a device that synthesizes it from the air, for pulmonary and cardiovascular diseases.Objective: to investigate the use of inhaled nitric oxide (Tianox device) in patients with MCI due to cerebrovascular (CVD) and neurodegenerative diseases (NDD) of the brain.Material and methods. We observed 36 patients (8 men, 28 women, mean age 66±8.9 years, from 50 to 76 years) with MCI that developed on the background of CVD and NDD. In addition to stroke prevention therapy, the patients with MCI received daily inhalation of a nitric oxideenriched air mixture via a Tianox device for 30 minutes. The patients had from 7 to 10 inhalation sessions (the first, experimental – 20 minutes, the following sessions – 30 minutes). Detailed neuropsychological tests were performed at baseline and 3 months after the end of treatment.Results. The therapy was well tolerated and no adverse events occurred. After 3 months, the average score on the Montreal Cognitive Assessment increased from 23.7±3.5 to 25.6±3.9 points (p<0.001), the ability to memorize 12 words – from 7.5±1.8 to 8.7±2.1 words (p<0.05), categorical associations – from 14.8±5.0 to 16.9±4.6 words (p<0.05), the number of words found in the Munsterberg test – from 14.9±5.8 to 18.1±5.8 (p<0.001).The emotional state of the patients improved, the signs of depression decreased according to the Beck Depression Inventory from 13.65±8.5 to 11.4±6.7 points (p<0.05), on the Hospital Anxiety and Depression Scale – from 8.6± 5.0 to 7.3±4.1 points (p<0.05); anxiety decreased on the Hospital Anxiety and Depression Scale – from 7.0±5.0 to 5.4±4.5 points (p<0.05), Insomnia Severity Index – from 11.1±7.9 to 7.8±6.3 points (p<0.05).Conclusion. Good tolerability and a positive effect of inhaled nitric oxide on CF and emotional state of patients with MCI against the background of CVD and NDD were found.

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Nitric oxide: from the mechanism of action to pharmacological effects in cerebrovascular diseases

Cited by 8 publications

References 31 publications

Astaxanthin inhibits homocysteine‑induced endothelial cell dysfunction via the regulation of the reactive oxygen species‑dependent VEGF‑VEGFR2‑FAK signaling pathway

Astaxanthin inhibits homocysteine‑induced endothelial cell dysfunction via the regulation of the reactive oxygen species‑dependent VEGF‑VEGFR2‑FAK signaling pathway

Involvement of Inducible Nitric Oxide Synthase in Pial Arterial Tone Formation under Metabolic Disorders and Streptozotocin-Induced Diabetes in Rats Kept on a High-Fat Diet

The use of inhaled nitric oxide (Tianox device) in patients with moderate cognitive impairment

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