Protective effects of beet (Beta vulgaris) leaves extract against oxidative stress in endothelial cells in vitro.

PMID: 

Phytother Res. 2020 Jan 27. Epub 2020 Jan 27. PMID: 31989717

Abstract Title: 

Protective effects of beet (Beta vulgaris) leaves extract against oxidative stress in endothelial cells in vitro.

Abstract: 

Beetroot is an herb used worldwide as a food product, raw material for food industry, ethanol production and source of food coloring. Beet leaves are an unconventional food with antioxidant properties, which might neutralize reactive oxygen species (ROS) induced by oxidized Low-Density Lipoprotein (LDL) present in dyslipidemias. This study aimed to elucidate the effects of beet leaves on the suppression of LDL oxidative processes. Beet leaves extract was produced, characterized, and tested for its antioxidant capacity using endothelial cells in vitro. A model of human umbilical vein endothelial cells was used in various tests, including viability assay, molecular analysis of antioxidant genes, ROS labeling, and macrophage adhesion assay. The extract improved the antioxidative protection of endothelial cells against different agents including oxidized LDL-cholesterol and HO. It acted on ROS directly due to its high content of natural antioxidants, but also due to the activation and improvement of cellular defenses such as Superoxide dismutase 1, Superoxide dismutase 2, and catalase. The inhibition of LDL-mediated oxidative effects on endothelial cells may turn this unconventional food a functional food with great potential for phytotherapy of atherosclerosis as an adjuvant for medicinal treatments.

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Chronic beetroot juice supplementation accelerates recovery kinetics following simulated match play in soccer players.

PMID: 

J Am Coll Nutr. 2020 Mar 3:1-9. Epub 2020 Mar 3. PMID: 32125249

Abstract Title: 

Chronic Beetroot Juice Supplementation Accelerates Recovery Kinetics following Simulated Match Play in Soccer Players.

Abstract: 

To assess the effect of beetroot juice (BET) on recovery kinetics of physical performance, muscle damage and perceived muscle soreness after simulated soccer match play in soccer players.In a randomized, double-blind, crossover design, thirteen soccer players completed the Loughborough Intermittent Shuttle Test LIST. Players received either BET or placebo (PLA) (2*150) for 7 days (3 days pre-exercise, on the day trial, and 3 days post-exercise). Physical performance (Squat jump: SJ, countermovement jump: CMJ, maximal voluntary contraction: MVC, and 20 meters sprint: SP), blood markers of muscle damage (creatine kinase: CK, Lactate dehydrogenase: LDH), inflammatory parameter (C-reactive protein: CRP) and perceived muscle soreness (DOMS) were assessed at baseline, 0 h, 24 h, 48 h and 72 h following the exercise.Following the LIST, a decrease was observed in CMJ, MVC and SP at 0 h, 24 h, 48 h in both conditions (p 

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A review of the biological effects of red beetroot and betalains.

PMID: 

Phytother Res. 2020 Mar 14. Epub 2020 Mar 14. PMID: 32171042

Abstract Title: 

Biological effects of red beetroot and betalains: A review.

Abstract: 

Over the past few years, the use of natural substances as protective or therapeutic agents has gained much attention worldwide. Recent modern studies have shown a variety of health benefits for red beetroot and its active compounds betalains (also betanin) such as antioxidative, anti-inflammation, anticancer, blood pressure and lipid lowering, also antidiabetic and anti-obesity effects. Betanin, the main component of the red beetroot, is a betalain glycosidic pigment, which is used as a food additive. This review summarizes findings in the literature and shows the therapeutic potential of red beetroot and its active compounds (betalains) as promising alternatives for supplemental therapies in multiple diseases.

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Lactobacillus rhamnosus GG supplementation modulates the gut microbiota to promote butyrate production, protecting against deoxynivalenol exposure.

PMID: 

Biochem Pharmacol. 2020 Feb 20 ;175:113868. Epub 2020 Feb 20. PMID: 32088259

Abstract Title: 

Lactobacillus rhamnosus GG supplementation modulates the gut microbiota to promote butyrate production, protecting against deoxynivalenol exposure in nude mice.

Abstract: 

Deoxynivalenol (DON) is the most common mycotoxin in grains, and DON exposure causes gastrointestinal inflammation and systemic immunosuppression. The immunosuppression caused by DON has raised serious concerns about whether it is safe to use probiotics in immunocompromised hosts. Gut microbiota remodeling by Lactobacillus is a potential effective strategy to prevent DON exposure. The athymic nude mice were chose as the model of immunocompromised animals. We tested the effect of the probiotic Lactobacillus rhamnosus GG (LGG) or Lactobacillus acidophilus (LA) supplementation on host protection against DON exposure and the underlying mechanisms in nude mice. DON exposure induced endoplasmic reticulum (ER) stress and impaired intestinal barrier function and microbiota, which were relieved by LGG supplementation but not LA supplementation. LGG supplementation significantly enhanced the intestinal barrier function, increased the body weight and the survival rate in nude mice that exposed to DON for two weeks. Furthermore, LGG supplementation modulated the gut microbiota by increasing the abundance of Bacteroidetes and the levels of the butyrate-producing genes But and Buk to promote butyrate production. Butyrate inhibited the IRE1α/XBP1 signaling pathway to reduce DON-induced intestine injury. In conclusion, LGG supplementation modulated the gut microbiota to promote butyrate production, protecting against DON exposure in nude mice. Both LGG and butyrate show promise for use in protecting against DON exposure.

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Anti-dengue infectivity evaluation of bioflavonoid from Azadirachta indica by dengue virus serine protease inhibition.

PMID: 

J Biomol Struct Dyn. 2020 Mar 9:1-14. Epub 2020 Mar 9. PMID: 32107969

Abstract Title: 

Anti-dengue infectivity evaluation of bioflavonoid fromby dengue virus serine protease inhibition.

Abstract: 

Dengue virus (DENV) serine protease enzyme, i.e. NS2B-NS3pro (non-structural protein 2B-non-structural protein 3) has been approved as prime drug target for the drug discovery against dengue infection, because of its essential role in viral replication. This study demonstrates the potential of bioflavonoids fromagainst dengue infection using computational and experimental approach. Initially, 49 bioflavonoids reported inwere collected and virtually screened on the catalytic triad of DENV protease, results in the identification of kaempferol-3-O-rutinoside (-9.555 kcal/mol), rutin (-9.324 kcal/mol), hyperoside (-7.879 kcal/mol), and epicatechin (-7.622 kcal/mol) as potent viral protease inhibitors against reference compound quercetin (-6.94 kcal/mol). Subsequently, these docked complexes were analyzed for the stability via molecular dynamics simulations and free binding energy calculations, suggested the considerable stability of selected bioflavonoids with viral protease. Additionally, density functional theory and ADMET (Absorption, Distribution, Metabolism, Excretion and Toxicity) analysis indicated the least chemical reactivity and considerable medicinal properties, respectively for the screened bioflavonoids by comparison to quercetin. Accordingly, kaempferol 3-O-β-rutinoside and epicatechin were evaluated at various concentrations for cell viability (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay) andantiviral activity (focus forming unit assay) against DENV-2 strain. The antiviral assay showed dose dependent inhibition of DENV-2 infectivity by the selected compounds while maximum 77.7% and 66.2% viral inhibition were recorded for 100 µM kaempferol 3-O-β-rutinoside and 1000 µM epicatechin, respectively without significant cell toxicity. These results suggested the potential of bioflavonoids fromin the development of effective drug against dengue infection.Communicated by Ramaswamy H. Sarma.

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Coenzyme Q10 improves the survival and reduces inflammatory markers in septic patients.

PMID: 

Bratisl Lek Listy. 2020 ;121(2):154-158. PMID: 32115970

Abstract Title: 

Coenzyme Q10 improves the survival and reduces inflammatory markers in septic patients.

Abstract: 

OBJECTIVE: This study aimed to evaluate the effect of Coenzyme Q10 (CoQ10) administration to patients in the early phase of sepsis to determine its effect on the markers of inflammation and the clinical outcomes of septic patients.BACKGROUND: Previous studies showed that CoQ10 levels were decreased in septic patients and worsening of mitochondrial dysfunction was observed.METHODS: In this randomized controlled trial septic patients (n=40) received 100 mg CoQ10 twice a day for seven days added to standard treatment of sepsis. As a primary endpoint levels of Interleukin 6 (IL-6), Tumor Necrosis Factor-α (TNF-α), Glutathione peroxidase and malondialdehyde (MDA) were assessed at baseline, third and 7th day after the intervention. Secondary endpoints included assessment of clinical scores and     in-hospital mortality.RESULTS: There was no difference in baseline inflammatory and oxidative injury markers between the groups. TNF-α and MDA levels decreased significantly in the CoQ10 group on the 7th day of the study (P:0.003 for both). There was a significant difference in the in-hospital mortality in the CoQ10 group compared to the control group (P:0.01).CONCLUSION: These findings suggest that CoQ10 has a positive effect on clinical parameters as well as mitochondrial dysfunction when administered in the early phase of sepsis (Tab. 2, Fig. 1, Ref. 38).

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Coenzyme Q10 reduces the deleterious cellular side effects of lead acetate.

PMID: 

Front Physiol. 2020 ;11:64. Epub 2020 Feb 7. PMID: 32116774

Abstract Title: 

Coenzyme Q10 Activates the Antioxidant Machinery and Inhibits the Inflammatory and Apoptotic Cascades Against Lead Acetate-Induced Renal Injury in Rats.

Abstract: 

The kidney is among the metabolic organs most susceptible to injury, particularly following exposure to xenobiotics and heavy metals. We aimed to explore the potential protective impacts of coenzyme Q10 (CoQ10) on lead acetate (PbAc)-induced nephrotoxicity in rats. Four experimental groups (= 7) were applied as follows: control group, CoQ10 alone (10 mg/kg), PbAc alone (20 mg/kg), and PbAc with CoQ10. Exposure to PbAc led to the accumulation of Pb in the kidney and increased urea and creatinine serum levels. The deposition of Pb coupled with the elevation of malondialdehyde and nitrate/nitrite levels along with the upregulation of inducible nitric oxide synthase. Additionally, upon PbAc poisoning, glutathione content and the antioxidant enzymes were depleted along with the downregulation of Nrf2 and HO-1 expression. Moreover, PbAc injection increased the protein and mRNA levels of pro-inflammatory cytokines namely, tumor necrosis factor-alpha and interleukin-1 beta, while decreased the levels of interleukin-10, an anti-inflammatory cytokine, in the kidney. Furthermore, exposure to PbAc correlated with increased levels of pro-apoptotic markers, Bax and caspase-3, and reduced levels of the anti-apoptotic marker Bcl-2. The administration of CoQ10 alleviated the molecular, biochemical and histological changes following PbAc intoxication. Thus, CoQ10 reduces the deleterious cellular side effects of PbAc exposure due to its antioxidant, anti-inflammatory and anti-apoptotic effects.

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Combination of omega 3 and coenzyme Q10 exerts neuroprotective potential against hypercholesterolemia-induced Alzheimer’s-like disease.

PMID: 

Neurochem Res. 2020 Mar 2. Epub 2020 Mar 2. PMID: 32124160

Abstract Title: 

Combination of Omega 3 and Coenzyme Q10 Exerts Neuroprotective Potential Against Hypercholesterolemia-Induced Alzheimer's-Like Disease in Rats.

Abstract: 

Alzheimer's disease (AD) is the most common form of dementia that progressively disrupts neurocognitive function, which has neither cure nor effective treatment. Hypercholesterolemia might be involved in brain alterations that could evolve into AD. The present study aims to evaluate the potential of omega-3, Co-enzyme Q10 (Co-Q10), as well as their combination in ameliorating hypercholesterolemia-initiated AD-like disease. We adapted a hypercholesterolemic (HC) rat model, a model of oxidative stress-mediated neurodegeneration, to study AD-like pathology. Hypercholesterolemia resulted in increased lipid peroxidation coupled with declined nitric oxide production, reduced glutathione levels, and decreased antioxidant activities of glutathione-s-transferase (GST) and glutathione peroxidase (GSH-Px) in the brain. Moreover, hypercholesterolemia resulted in decreased acetylcholine (ACh) levels and increased acetylcholine-esterase (AChE) activity, along with an increment of tumor necrosis factor and amyloid-β 42. Behaviorally, HC-rats demonstrated depressive-like behavior and declined memory. Treatment of HC-rats with omega-3 and Co-Q10 (alone or in combination) alleviated the brain oxidative stress and inflammation, regulated cholinergic functioning, and enhanced the functional outcome. These findings were verified by the histopathological investigation of brain tissues. This neuroprotective potential of omega-3 and Co-Q10 was achieved through anti-oxidative, anti-inflammatory, anti-amyloidogenic, pro-cholinergic, and memory-enhancing activities against HC-induced AD-like disease; suggesting that they may be useful as prophylactic and therapeutic agents against the neurotoxic effects of hypercholesterolemia.

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Coenzyme Q10 in association with metabolism-related AMPK/PFKFB3 and angiogenic VEGF/VEGFR2 genes in breast cancer patients.

PMID: 

Mol Biol Rep. 2020 Mar 5. Epub 2020 Mar 5. PMID: 32140960

Abstract Title: 

Coenzyme Q10 in association with metabolism-related AMPK/PFKFB3 and angiogenic VEGF/VEGFR2 genes in breast cancer patients.

Abstract: 

Low levels of coenzyme Q10 (CoQ10) have been reported in the circulation of patients with breast cancer, particularly in metastatic features. Our objective was to study the correlation between plasma levels of CoQ10 and the tumoral expression levels of AMPK, PFKFB3, VEGF, and VEGFR2. This study was a part of consecutive case series conducted on 100 women with newly diagnosed invasive ductal breast carcinoma, with an age range of 30-60 years. Plasma levels of CoQ10 were measured using HPLC coupled to an UV detector. The expression levels were quantified using quantitative real-time PCR. Structural equation modeling (SEM) was applied to generate pathways describing gene-to-gene inter-correlations. Using SEM identified AMPK expression to contribute positively to VEGF-A/VEGFR2 ratio (coefficient b = 0.64, P 

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Coenzyme-Q10 exerts hepatoprotective effect in fructose-induced fatty liver model.

PMID: 

Pharmacol Rep. 2020 Mar 10. Epub 2020 Mar 10. PMID: 32157594

Abstract Title: 

CoQ10 exerts hepatoprotective effect in fructose-induced fatty liver model in rats.

Abstract: 

BACKGROUND: Excess dietary sugar is associated with deleterious metabolic effects, liver injury, and coenzyme-Q10 (CoQ10) deficiency. This study investigates the ability of CoQ10 to protect against fructose-induced hepatic damage.METHODS: Rats were fed tap water or 30% fructose for 12 weeks with or without CoQ10 (10 mg/kg, po). An additional group of rats were allowed to feed on either water or 30% fructose for 12 weeks, followed by four weeks of treatment with either the vehicle or CoQ10.RESULTS: Fructose-fed rats showed lower CoQ10 levels, increased systolic pressure, increased body weight, higher liquid consumption, decreased food intake and hyperglycemia. Fructose-fed rats also showed deteriorated serum and liver lipid profiles, impaired liver function tests and oxidative status, and lower expression of adiponectin receptor 1 and 2 along with higher GLUT-2 levels. Furthermore, following fructose treatment, tyrosine kinase-PI3K pathway was inhibited. Additionally, there was an increase in the levels of apoptotic markers and serum visfatin and a decrease in the levels of adiponectin and soluble receptor of the advanced glycated end product. Consequently, several histopathological changes were detected in the liver. Concurrent or three months post-exposure administration of CoQ10 in fructose rats significantly reversed or attenuated all the measured parameters and hepato-cytoarchitecture alterations.CONCLUSION: This study suggests CoQ10 supplement as a possible prophylaxis or treatment candidate for fructose-induced liver injury.

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