This study aimed to test the effect of n-3 polyunsaturated fatty acid (PUFA)-enriched hen egg consumption on serum lipid and free fatty acid profiles, inflammatory and oxidative stress biomarkers, and microvascular reactivity in patients with coronary artery disease (CAD). Forty CAD patients participated in this study. Of those, 20 patients had acute CAD (Ac-CAD), and 20 patients had chronic CAD (Ch-CAD). The control group (N = 20) consumed three regular hen eggs/daily (249 mg n-3 PUFAs/day), and the n-3 PUFAs group (N = 20) consumed three n-3 PUFA-enriched hen eggs/daily (1053 g n-3 PUFAs/day) for 3 weeks. Serum n-3 PUFA concentration significantly increased (in all CAD patients), while LDL cholesterol and IL-6 (in Ac-CAD patients), and hsCRP and IL-1a (in all CAD patients) significantly decreased in the n-3 PUFAs group. Glutathione peroxidase (GPx) activity significantly decreased, and forearm skin microvascular reactivity in response to vascular occlusion (postocclusive reactive hyperemia (PORH)) remained unchanged in both the n-3 PUFAs and control groups in total CAD, Ac-CAD, and Ch-CAD patients. Potentially, n-3 PUFA-enriched hen eggs can change the free fatty acid profile to a more favorable lower n6/n3 ratio, and to exhibit mild anti-inflammatory effects but not to affect microvascular reactivity in CAD patients.

High salt (HS) dietary intake leads to impaired vascular endothelium-dependent responses to various physiological stimuli, some of which are mediated by arachidonic acid (AA) metabolites. Transgenic Tff3^−/− gene knockout mice (Tff3^−/−/C57BL/6N) have changes in lipid metabolism which may affect vascular function and outcomes of stroke. We aimed to study the effects of one week of HS diet (4% NaCl) on vascular function and stroke induced by transient occlusion of middle cerebral artery in Tff3^−/− and wild type (WT/C57BL/6N) mice. Flow-induced dilation (FID) of carotid artery was reduced in WT-HS mice, but not affected in Tff3^−/−-HS mice. Nitric oxide (NO) mediated FID. NO production was decreased with HS diet. On the contrary, acetylcholine-induced dilation was significantly decreased in Tff3^−/− mice on both diets and WT-HS mice. HS intake and Tff3 gene depletion affected the structural components of the vessels. Proteomic analysis revealed a significant effect of Tff3 gene deficiency on HS diet-induced changes in neuronal structural proteins and acute innate immune response proteins’ expression and Tff3 depletion, but HS diet did not increase the stroke volume, which is related to proteome modification and upregulation of genes involved mainly in cellular antioxidative defense. In conclusion, Tff3 depletion seems to partially impair vascular function and worsen the outcomes of stroke, which is moderately affected by HS diet.

Introduction: It is well documented that high-salt (HS) diet increases systemic and vascular oxidative stress in various animal models and in humans, leading to impairment of vascular reactivity. The present study examined the interaction of genotype and HS diet intake and the potential effects of oxidative stress – antioxidative system balance on the flow-induced dilation (FID) in pressurized carotid arteries of normotensive Tff3−/−/C57BL/6N knockout mice and their wild-type (WT) controls. Methods: Male, ten-week-old transgenic Tff3−/−/C57BL/6N (Tff3−/−) knockout mice and WT/C57BL/6N (WT) (parental strain) healthy mice were divided in LS (0.4% NaCl in rodent chow) and HS (4% NaCl in rodent chow fed for 1 week) groups. Additionally, LS and HS groups were treated with 1 mmol/L 4-hydroxy-2,2,6,6-tetramethylpiperidin-1-oxyl (TEMPOL) dissolved in the drinking water. After anesthesia with ketamine chloride (100 mg/kg) and midazolam (5 mg/kg), blood pressure was measured, carotid arteries and aortas were isolated, and blood samples were collected. Results: FID was decreased in WT_HS mice and restored by superoxide scavenger TEMPOL in vivo. On the other hand, attenuated FID of Tff3−/− mice was not further affected by HS diet or TEMPOL in vivo treatment. Vascular superoxide/reactive oxygen species levels were increased with HS diet in both strains and restored by TEMPOL. HS upregulated glutathione peroxidase 1 (GPx1) gene expression in WT_HS and Tff3−/−_HS mice, while GPx activity was significantly decreased only in WT_HS group. Systemic (serum) markers of oxidative stress (oxLDL and AOPP) and arterial blood pressure were similar among groups. Conclusion: HS diet increases vascular oxidative stress and impairs vasodilation in WT mice. Tff3 gene deficiency attenuates vasodilation per se, without further effects of HS intake. This can be attributed to vascular upregulation of antioxidative enzyme GPx1 in Tff3−/−/C57BL/6N mice conferring protection from oxidative stress.

Backgrounds/Objectives: Following previous findings on high-salt (HS)-intake-related increase of oxidative stress, this study explored whether carnosine (CAR; β-alanyl-L-histidine), a reactive oxygen species (ROS) scavenger, enhanced antioxidative defence and vascular function following HS, potentially via the NRF2 or HIF-1α signalling pathway. Methods: Sprague Dawley rats (64, 8–10 weeks old, both sexes) were divided into four groups (n = 6/group): CTRL (0.4% NaCl), HS (4% NaCl for 7 days), CTRL + CAR (0.4% NaCl and 150 mg/kg/day oral CAR supplementation), and HS + CAR (4% NaCl and CAR). Acetylcholine-induced relaxation (AChIR) and hypoxia-induced relaxation (HIR) were evaluated in norepinephrine-precontracted (NE, 10⁻⁷ M) aortic rings. HIR was also tested with NRF2 (ML-385, 5 × 10⁻⁶ M) and HIF-1α (LW6, 10⁻⁴ M) inhibitors. Gene expression of superoxide dismutases 1, 2, and 3 (SOD1, 2 and 3), glutathione peroxidases (GPx1 and 4), catalase (CAT), NRF2, and NAD(P)H dehydrogenase (quinone 1) (NQO1) in aortic tissue was measured by RT-qPCR. Ferric reducing antioxidant power (FRAP) and advanced oxidation protein products (AOPPs) assays were performed on serum samples. All experimental procedures conformed to the European Guidelines (directive 86/609) and were approved by the local and national Ethical Committees (#2158-61-46-23-36, EP355/2022). Results: HS impaired AChIR and HIR, both preserved by CAR. NRF2 and HIF-1α inhibitors suppressed HIR in the HS and HS + CAR groups. CAR significantly increased SOD1 and 2, NRF2, and NQO1 expression and SOD activity compared to the CTRL and HS groups. GPx1 and GPx4 were upregulated in HS + CAR compared to HS. CAR prevented an increase in AOPPs, which were elevated in HS, while FRAP was highest in HS + CAR. Conclusions: Carnosine enhances antioxidative defence by upregulating antioxidant enzymes and activities and preserves vascular relaxation, likely via NRF2 signalling.

The aim of this clinical study was to determine the impact of the consumption of chicken eggs enriched with n-3 polyunsaturated fatty acids, selenium, vitamin E, and lutein on micro- and macrovascular endothelium-dependent dilation, inflammation biomarkers, and oxidative stress levels in participants with chronic coronary syndrome (CCS). This was a double-blind, placebo-controlled clinical study that included 30 CCS participants (9 women, 21 men) randomized into the control group (N = 15), who ate ordinary chicken eggs (three per day), and the Nutri4 group (N = 15), who ate enriched eggs (three per day) for 21 days. Microvascular and macrovascular endothelium-dependent vasodilation was evaluated by measuring forearm skin post-occlusive reactive hyperemia (PORH) and acetylcholine-induced dilation (AChID) and the flow-mediated dilation (FMD) of the brachial artery, respectively. The serum lipid profile, anti- and proinflammatory cytokine levels, serum concentration of nitric oxide synthase (NOS) isoforms, and oxidative stress biomarkers were measured before and after the diet protocols. Enriched, but not regular, chicken eggs significantly improved microvascular PORH and AChID and macrovascular FMD, increased the serum concentration of inducible NOS, decreased serum triglyceride levels, and decreased proinflammatory cytokine IL-17A and TGF-1β levels compared to initial measurements. Patients with CCS can benefit from the consumption of enriched chicken eggs due to improved lipid biomarkers, a more favorable anti-inflammatory milieu, and improved vascular relaxation at micro- and macrovascular levels.