Risk factors related to cardiovascular diseases and the metabolic syndrome in multiple sclerosis – a systematic review

Wens, Inez; Dalgas, Ulrik; Stenager, Egon; Eijnde, Bert O.

doi:10.1177/1352458513504252

Cited by 103 publications

(88 citation statements)

References 60 publications

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“…Cardiovascular diseases (CVDs) have high mortality rates worldwide and have become a serious burden in many countries [1, 2]. Atherosclerosis (AS) is a progressive condition involving accumulation of lipids and fibrous elements in the large arteries, which is a key trigger for CVD [3].…”

Section: Introductionmentioning

confidence: 99%

Allicin Decreases Lipopolysaccharide-Induced Oxidative Stress and Inflammation in Human Umbilical Vein Endothelial Cells through Suppression of Mitochondrial Dysfunction and Activation of Nrf2

Zhang¹,

Pan²,

Xu³

et al. 2017

Cell Physiol Biochem

103

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Background: Allicin, a major component of garlic, is regarded as a cardioprotective agent and is associated with increased endothelial function. Methods: The effects of allicin on lipopolysaccharide (LPS)-induced vascular oxidative stress and inflammation in cultured human umbilical vein endothelial cells (HUVECs) and the mechanisms underlying these effects were studied. The protective effects were measured using cell viability, a lactate dehydrogenase (LDH) assay and cell apoptosis as indicators, and the anti-oxidative activity was determined by measuring reactive oxygen species (ROS) generation, oxidative products and endogenous antioxidant enzyme activities. HUVEC mitochondrial function was assessed by determining mitochondrial membrane potential (MMP) collapse, cytochrome c production and mitochondrial ATP release. To investigate the potential underlying mechanisms, we also measured the expression of dynamic mitochondrial proteins using western blotting. Furthermore, we evaluated the Nrf2 antioxidant signaling pathway using an enzyme-linked immunosorbent assay (ELISA). Results: Our results demonstrated that allicin enhanced HUVEC proliferation, which was suppressed by LPS exposure, and LDH release. Allicin ameliorated LPS-induced apoptosis, suppressed ROS overproduction, reduced lipid peroxidation and decreased the endogenous antioxidant enzyme activities in HUVECs. These protective effects were associated with the inhibition of mitochondrial dysfunction as indicated by decreases in the MMP collapse, cytochrome c synthesis and mitochondrial ATP release. In addition, allicin attenuated the LPS-induced inflammatory responses, including endothelial cell adhesion and TNF-α and IL-8 production. Furthermore, allicin increased the expression of LXRα in a dose-dependent manner. Allicin-induced attenuation of inflammation was inhibited by LXRα siRNA treatment. Finally, allicin activated NF-E2-related factor 2 (Nrf2), which controls the defense against oxidative stress and inflammation. Conclusions: Taken together, the present data suggest that allicin attenuated the LPS-induced vascular injury process, which may be closely related to the oxidative stress and inflammatory response in HUVECs. Allicin modulated Nrf2 activation and protected the cells against LPS-induced vascular injury. Our findings suggest that allicin attenuated the LPS-induced inflammatory response in blood vessels.

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Section: Introductionmentioning

confidence: 99%

Allicin Decreases Lipopolysaccharide-Induced Oxidative Stress and Inflammation in Human Umbilical Vein Endothelial Cells through Suppression of Mitochondrial Dysfunction and Activation of Nrf2

Zhang¹,

Pan²,

Xu³

et al. 2017

Cell Physiol Biochem

103

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“…Increased homocysteine and decreased folate decrease S-adenosylmethionine, in turn depriving the methyl source that is necessary for melatonin formation from NAS. Increased homocysteine and decreased melatonin would then contribute to elevated risk of cardiovascular disorders in MS (Wens et al, 2013). As such, increased homocysteine and decreased folate, as with increased TNF-α, contribute to decreased melatonin in MS.…”

Section: Melatoninergic Pathway Regulationmentioning

confidence: 97%

Multiple sclerosis: The role of melatonin and N-acetylserotonin

Anderson¹,

Rodriguez

2015

Multiple Sclerosis and Related Disorders

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Multiple sclerosis (MS) is an immune mediated disorder that is under intensive investigation in an attempt to improve on available treatments. Many of the changes occurring in MS, including increased mitochondrial dysfunction, pain reporting and depression may be partly mediated by increased indoleamine 2,3-dioxygenase, which drives tryptophan to the production of neuroregulatory tryptophan catabolites and away from serotonin, N-acetylserotonin and melatonin production. The consequences of decreased melatonin have classically been attributed to circadian changes following its release from the pineal gland. However, recent data shows that melatonin may be produced by all mitochondria containing cells to some degree, including astrocytes and immune cells, thereby providing another important MS treatment target. As well as being a powerful antioxidant, anti-inflammatory and antinociceptive, melatonin improves mitochondrial functioning, partly via increased oxidative phosphorylation. Melatonin also inhibits demyelination and increases remyelination, suggesting that its local regulation in white matter astrocytes by serotonin availability and apolipoprotein E4, among other potential factors, will be important in the etiology, course and treatment of MS. Here we review the role of local melatonin and its precursors, N-acetylserotonin and serotonin, in MS.

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“…6 Notably, dietary fats and oils can cause hyperlipidemia, and thereby induce ischemic and hemorrhagic strokes. Many studies have compared the effects of various vegetable oils on the lifespan of stroke-prone spontaneously hypertensive rats (SHR-SP), an animal model of sodium salt-sensitive hypertension and cerebral stroke.…”

Section: Introductionmentioning

confidence: 99%

Comparative effects of plant oils on the cerebral hemorrhage in stroke-prone spontaneously hypertensive rats

Cai

Jang

Kim

et al. 2014

Nutritional Neuroscience

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Risk factors related to cardiovascular diseases and the metabolic syndrome in multiple sclerosis – a systematic review

Cited by 103 publications

References 60 publications

Allicin Decreases Lipopolysaccharide-Induced Oxidative Stress and Inflammation in Human Umbilical Vein Endothelial Cells through Suppression of Mitochondrial Dysfunction and Activation of Nrf2

Allicin Decreases Lipopolysaccharide-Induced Oxidative Stress and Inflammation in Human Umbilical Vein Endothelial Cells through Suppression of Mitochondrial Dysfunction and Activation of Nrf2

Multiple sclerosis: The role of melatonin and N-acetylserotonin

Comparative effects of plant oils on the cerebral hemorrhage in stroke-prone spontaneously hypertensive rats

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