alpha-carotene has been researched along with Inflammation* in 4 studies
1 trial(s) available for alpha-carotene and Inflammation
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Short term effects of palm-tocotrienol and palm-carotenes on vascular function and cardiovascular disease risk: A randomised controlled trial.
In vitro, ex vivo and animal studies suggest palm-based tocotrienols and carotenes enhance vascular function, but limited data in humans exists. The aim was to examine the effects of palm-tocotrienols (TRF- 80) and palm-carotene (CC-60) supplementation on vascular function and cardiovascular disease (CVD) risk factors in adults at increased risk of impaired vascular function.. Plasma α- and β-carotene and α-, δ- and γ-tocotrienol concentrations increased in CC-60 and TRF-80 groups, respectively, compared to placebo (mean ± SE difference in total plasma carotene change between CC-60 and placebo: 1.5 ± 0.13 μg/ml, p < 0.0001; total plasma tocotrienol change between TRF-80 and placebo: 0.36 ± 0.05 μg/ml, p < 0.0001). Neither FMD (treatment x time effect for CC-60 vs. placebo, p = 0.71; TRF-80 vs. placebo, p = 0.80) nor any other vascular function and CVD outcomes were affected by treatments.. CC-60 and TRF-80 supplementation increased bioavailability of palm-based carotenes and tocotrienols but had no effects, superior or detrimental, on vascular function or CVD risk factors. Topics: Adolescent; Adult; Aged; beta Carotene; Blood Glucose; Brachial Artery; Cardiovascular Diseases; Carotenoids; Diabetes Mellitus, Type 2; Dietary Supplements; Double-Blind Method; Female; Humans; Inflammation; Insulin; Male; Middle Aged; Oxidative Stress; Palm Oil; Risk Factors; Tocotrienols; Young Adult | 2016 |
3 other study(ies) available for alpha-carotene and Inflammation
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Carotenoids Inhibit Fructose-Induced Inflammatory Response in Human Endothelial Cells and Monocytes.
This research is aimed at determining the vascular health characteristics of carotenoids by evaluating their effect on excessive inflammatory response in endothelial and monocyte cells, the main factors of atherosclerosis.. Human umbilical vein endothelial cells (HUVECs) or U937 monocytes were treated with escalating concentrations (0.1, 0.5, and 1 . Carotenoids repressed monocyte adhesion to fructose-stimulated ECs dose dependently via decreasing primarily the expression of endothelial VCAM-1. In ECs and monocytes, three carotenoids, i.e.,. Our results show that carotenoids have a variety of anti-inflammatory and antiatherosclerosis activities, which can help prevent or reduce fructose-induced inflammatory vascular diseases. Topics: Atherosclerosis; Beta-Cryptoxanthin; Carotenoids; Cell Adhesion; Cytokines; Endothelial Cells; Fructose; Human Umbilical Vein Endothelial Cells; Humans; Inflammation; Lipid Peroxidation; Lutein; Lycopene; Monocytes; Oxidative Stress; Reactive Oxygen Species; U937 Cells | 2020 |
Evaluation of Antioxidant Intakes in Relation to Inflammatory Markers Expression Within the Normal Breast Tissue of Breast Cancer Patients.
Chronic inflammation may be a causative factor in breast cancer. One possible underlying mechanism is the generation of oxidative stress, which may favor tumorigenic processes. Antioxidant consumption may, therefore, help reduce tissue inflammation levels. However, few studies have explored this relation in breast tissue. We aimed to evaluate correlations between antioxidant (vitamin A/retinol, vitamin C, vitamin E, β-carotene, α-carotene, lycopene, lutein/zeaxanthin, β-cryptoxanthin, selenium, and zinc) intakes and protein expression levels of interleukin (IL)-6, tumor necrosis factor-α, C-reactive protein, cyclooxygenase-2, leptin, serum amyloid A1, signal transducer and activator of transcription 3, IL-8, IL-10, lactoferrin, and transforming growth factor-β measured in the normal breast tissue of 160 women diagnosed with breast cancer. Antioxidant intakes were collected using a self-administered food frequency questionnaire. Inflammation marker expression was assessed by immunohistochemistry. Correlations between antioxidant intakes and inflammatory marker expression were evaluated using Spearman's partial correlation coefficients ( r) for all women and for premenopausal and postmenopausal women separately. After Bonferroni correction, negative correlations were observed between dietary β-tocopherol and IL-10 expression in all women combined ( r = -0.26, P = .003) and among postmenopausal women ( r = -0.39, P = .003). For all women, a negative correlation was found between total zinc intakes and IL-10 ( r = -0.26, P = .002). Among postmenopausal women, dietary selenium intake was negatively correlated with the expression of lactoferrin ( r = -0.39, P = .003). No associations were observed in premenopausal women. Our findings suggest that consumption of specific antioxidants, including β-tocopherol, zinc, and selenium, may act on the breast tissue through mechanisms affecting the expression of some inflammation markers, particularly among postmenopausal women. Topics: Antioxidants; Biomarkers; Breast; Breast Neoplasms; Carotenoids; Diet; Female; Humans; Inflammation; Interleukin-6; Lycopene; Middle Aged; Oxidative Stress; Postmenopause; Premenopause; Selenium; Zinc | 2017 |
Plasma levels of lipophilic antioxidant vitamins in acute ischemic stroke patients: correlation to inflammation markers and neurological deficits.
Acute ischemic stroke is a clinical condition accompanied by inflammation and oxidative stress. In this study, we compared levels of plasma lipophilic antioxidants and inflammation markers between patients with stroke and healthy controls and assessed the associations of antioxidants, inflammation markers, and neurologic deficits among patients with stroke.. We measured plasma levels of lipophilic antioxidant vitamins (retinol, lycopene, alpha-carotene, beta-carotene, alpha-tocopherol, and gamma-tocopherol), inflammation markers (high-sensitivity C-reactive protein [hs-CRP], fibrinogen, erythrocyte sedimentation rate, and white blood cell count), and neurologic deficits (indicated by the score of the National Institute of Health Stroke Scale) in 68 patients with acute ischemic stroke within 48 h after stroke onset in comparison with 41 normal controls.. Plasma alpha- and beta-carotene concentrations were lower and levels of inflammation markers were higher among patients with acute ischemic stroke compared with normal controls. Levels of alpha- and beta-carotene in patients with stroke were negatively associated with hs-CRP level (R = -0.29 and -0.41, respectively, P < 0.01) and with neurologic deficits (R = -0.28 and -0.27, respectively, P < 0.05). The negative association between neurologic deficits and combined plasma levels of alpha- and beta-carotene remained after adjustment for age and sex (P = 0.04). However, the magnitude of association decreased after adjustment of hs-CRP (P = 0.08).. Plasma concentrations of alpha- and beta-carotene are lower in patients with acute ischemic stroke than in healthy controls and are negatively correlated with hs-CRP level and neurologic deficits. The negative association between neurologic deficits and combined plasma alpha- and beta-carotene levels is confounded by hs-CRP. Topics: Acute Disease; Aged; Antioxidants; beta Carotene; Biomarkers; Brain Ischemia; C-Reactive Protein; Carotenoids; Case-Control Studies; Disease Progression; Female; Humans; Inflammation; Lipid Peroxidation; Male; Middle Aged; Nutritional Status; Oxidative Stress; Severity of Illness Index; Vitamin A; Vitamins | 2005 |