PMID: 

Food Funct. 2018 Nov 14 ;9(11):5653-5659. PMID: 30302465

Abstract Title: 

Ubiquinol is superior to ubiquinone to enhance Coenzyme Q10 status in older men.

Abstract: 

Coenzyme Q10 (CoQ10) exerts its functions in the body through the ability of its benzoquinone head group to accept and donate electrons. The primary functions are to relay electrons for ATP production in the electron transport chain and to act as an important lipophilic antioxidant. Ubiquinone, the oxidized form of CoQ10, is commonly formulated in commercial supplements, and it must be reduced to ubiquinol to exert CoQ10's functions after consumption. Thus, we aimed to examine whether as compared to ubiquinone, ubiquinol would be more effective to enhance the CoQ10 status in older men. We conducted a double-blind, randomized, crossover trial with two 2-week intervention phases and a 2-week washout between crossovers. Ten eligible older men were randomized to consume either the ubiquinol or ubiquinone supplement at a dose of 200 mg d-1 with one of the main meals. A total of 4 blood samples were collected after an overnight fast for the determination of ubiquinone and ubiquinol in plasma and PBMC and the assessment of FRAP, total thiol, and malondialdehyde (MDA) in plasma and ATP in PBMC. After 2 weeks of the supplementation, the ubiquinol supplement significantly increased plasma ubiquinone 1.7 fold from 0.2 to 0.6μmol L-1 and total CoQ10 (the sum of 2 forms) 1.5 fold from 1.3 to 3.4 μmol L-1 (p

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PMID: 

Br J Hosp Med (Lond). 2019 Oct 2 ;80(10):589-593. PMID: 31589506

Abstract Title: 

Supplementation with selenium and coenzyme Q10 in critically ill patients.

Abstract: 

Multiple organ dysfunction and resultant mortality in critically ill patients has been linked with impaired cellular energy supply and oxidative stress. Clinical studies supplementing selenium, on the basis of its role as a key cofactor of antioxidant enzymes, have reported variable outcomes in critically ill patients. However, the synergistic interaction between selenium and coenzyme Q10, which has essential roles in cellular energy supply and as an antioxidant, has not been considered in such studies. This article reviews the link between selenium and coenzyme Q10, and the potential role of their co-supplementation in critical illness.

PMID: 

J Lab Physicians. 2019 Oct-Dec;11(4):317-322. PMID: 31929697

Abstract Title: 

Endothelial dysfunction and inflammatory biomarkers as a response factor of concurrent coenzyme Q10 add-on metformin in patients with type 2 diabetes mellitus.

Abstract: 

OBJECTIVES: The objective of the study was to evaluate the effect of metformin alone or in combination with coenzyme Q10 (CoQ10) on inflammatory changes and endothelial dysfunction in patients with type 2 diabetes mellitus (T2DM).MATERIALS AND METHODS: A total numbers of 54 patients with T2DM compared to 30 healthy subjects were divided into three groups: Group A (= 30): healthy subjects without any medications; Group B (= 24): T2DM patients treated with metformin 1 g/day; and Group C (= 30): T2DM patients treated with metformin 1 g/day plus CoQ10, 300 mg/day. The duration of the study was 8 weeks. Fasting blood glucose, glycated hemoglobin, lipid profile, blood pressure variables, fasting insulin, insulin resistance, homeostatic model assessment of insulin resistance, vascular cell adhesion molecule 1 (VCAM-1), and E-selectin were measured before and after therapy.RESULTS: Metformin and/or CoQ10 therapy illustrated an insignificant effect on the fody mass index. This combination produced a significant improvement of metabolic changes in patients with T2DM (

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PMID: 

Res Pharm Sci. 2019 Dec ;14(6):524-533. Epub 2019 Dec 11. PMID: 32038732

Abstract Title: 

Possible antioxidant mechanism of coenzyme Q10 in diabetes: impact on Sirt1/Nrf2 signaling pathways.

Abstract: 

Oxidative stress is a major complication in diabetes mellitus. The aim of this study was to investigate potential antioxidant activity of coenzyme Q10 (Co Q10) against hyperglycemia-induced oxidative stress in diabetic rat and unraveling its mechanism of action by focusing on silent information regulator 1 (Sirt1) and nuclear factor E2-related factor 2 (Nrf2) mRNA expression level. Furthermore, the activity of two Nrf2-dependent antioxidant enzymes (superoxide dismutase and catalase) in the liver of diabetic rats was studied. After induction of diabetes in rats using streptozotocin (55 mg/kg), rats were divided into five groups of six each. Groups 1 and 2 (healthy control groups) were injected with isotonic saline or sesame oil; group 3 received Co Q10 (10 mg /Kg /day), group 4, as a diabetic control, received sesame oil; and group 5 was diabetic rats treated with Co Q10. Afterwards, serum and liver samples were collected, and oxidative stress markers, lipid profile, as well as the expression of Sirt1 and Nrf2 genes were measured. Diabetes induction significantly reduced expression level of Sirt1 and Nrf2 mRNAs and also declined catalase, superoxide dismutase activities, and total thiol groups levels in diabetic group in comparison to healthy controls, while a significant increase was found in the levels of malondialdehyde and lipid profile. Co Q10 treatment significantly up-regulated Sirt1 and Nrf2 mRNA levels along with an increase in catalase activity in diabetic group as compared with untreated diabetic rats. Furthermore, Co Q10 caused a marked decrease in malondialdehyde levels and significantly improved lipid profile. Our data demonstrated that Co Q10 may exert its antioxidant activity in diabetes through the induction of Sirt1/Nrf2 gene expression.

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PMID: 

Phytother Res. 2020 Feb 3. Epub 2020 Feb 3. PMID: 32017253

Abstract Title: 

Effect of curcumin supplementation on disease severity in patients with liver cirrhosis: A randomized controlled trial.

Abstract: 

Recent reports indicated that curcumin had beneficial effects in animal models of liver injury and cirrhosis. Current study aimed to investigate the effects of curcumin supplementation in patients with liver cirrhosis. In this randomized double-blind placebo-controlled trial, 70 patients with liver cirrhosis aged 20-70 years were randomly divided into two groups to receive 1,000 mg/day curcumin (n = 35) or placebo (n = 35) for 3 months. Model for end-stage liver disease (MELD) (i), MELD, MELD-Na, and Child-Pugh scores were used to assess the severity of cirrhosis. Sixty patients (29 in the curcumin group and 31 in the placebo group) completed the study. MELD(i) (15.55 ± 3.78 to 12.41 ± 3.07), MELD (15.31 ± 3.07 to 12.03 ± 2.79), MELD-Na (15.97 ± 4.02 to 13.55 ± 3.51), and Child-Pugh (7.17 ± 1.54 to 6.72 ± 1.31) scores decreased significantly in the curcumingroup after 3-month intervention (p

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PMID: 

J Laryngol Otol. 2020 Feb 7:1-6. Epub 2020 Feb 7. PMID: 32029014

Abstract Title: 

Role of turmeric extract in minimising mucositis in patients receiving radiotherapy for head and neck squamous cell cancer: a randomised, placebo-controlled trial.

Abstract: 

OBJECTIVE: To determine the role of turmeric extract in reducing mucositis in patients undergoing radiotherapy for head and neck cancer.METHODS: Sixty-one patients who underwent radiotherapy were included in the study and randomised into groups A and B. Patients in group A received 500 mg of turmeric extract (BCM-95) thrice daily, while patients in group B received placebo until radiotherapy completion. All patients were assessed for oral mucositis on a weekly basis during treatment and two months post-treatment using the National Cancer Institute Common Terminology Criteria for Adverse Events and World Health Organization criteria.RESULTS: Both groups had a similar grade of mucositis in first two weeks of treatment. The severity of mucositis was progressive in the control group, with four patients developing grade 3 mucositis by week four. In group A, however, the majority of patients (73.3 per cent) had grade 1 mucositis after four weeks of treatment. The difference was statistically significant from the third week onwards (p

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PMID: 

Molecules. 2020 Feb 7 ;25(3). Epub 2020 Feb 7. PMID: 32046055

Abstract Title: 

Curcumin, an Active Constituent of Turmeric Spice: Implication in the Prevention of Lung Injury Induced by Benzo(a) Pyrene (BaP) in Rats.

Abstract: 

Benzo(a)pyrene (BaP) is a well-known carcinogen and enhances oxidative stress and apoptosis and also alters several molecular pathways. Curcumin is an active ingredient of, and it has potent anti-inflammatory, antioxidant activity that defends cells from oxidative stress and cell death. The objectives of the present study were to explore the protective effects of curcumin against long-term administration of BaP induced disturbances in lungs of rats. Male rats were randomly divided into four groups: saline control, BaP only, BaP + curcumin, and curcumin only. Lung histopathology, electron microscopy, inflammatory cytokine release, antioxidant levels, apoptosis, and cell cycle were examined. Instillation of BaP significantly increased infiltration of inflammatory cells in alveolar space and inflammatory cytokine in blood. BaP induced lung tissue alterations including mild bronchitis, scant chronic inflammatory cell infiltrate in the wall of the respiratory bronchiole, and mild intra-alveolar haemorrhage. However, these alterations were found to be significantly less as mild inflammatory cell infiltrate in curcumin plus BaP treated group. Furthermore, electron microscopy results also showed necrotic changes and broken cell membrane of Type-II epithelial cell of alveoli in BaP group, which was reduced after adding curcumin treatment. In addition, we found BaP plus curcumin treatment effectively reduced inflammatory cytokines Tumour Necrosis Factor alpha (TNF-α), Interleukin 6 (IL-6), and C-reactive protein (CRP) levels in blood serum. Moreover, the levels of tunnel staining and p53 expression were significantly increased by BaP, whereas these changes were noticeably modulated after curcumin treatment. BaP also interferes in normal cell cycle, which wassignificantly improved with curcumin treatment. Overall, our findings suggest that curcumin attenuates BaP -induced lung injury, probably through inhibiting inflammation, oxidative stress and apoptosis in lung epithelial cells, and improving cell proliferation and antioxidants level. Thus, curcuminmay be an alternative therapy for improving the outcomes of Benzo(a)pyrene-induced lung injury.

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PMID: 

Int J Mol Sci. 2019 Feb 26 ;20(5). Epub 2019 Feb 26. PMID: 30813635

Abstract Title: 

Mechanisms of PKC-Mediated Enhancement of HIF-1α Activity and its Inhibition by Vitamin K2 in Hepatocellular Carcinoma Cells.

Abstract: 

Hypoxia-inducible factor 1 (HIF-1) plays important roles in cancer cell biology. HIF-1α is reportedly activated by several factors, including protein kinase C (PKC), in addition to hypoxia. We investigated the role of PKC isoforms and the effects of vitamin K2 (VK2) in the activation process of HIF-1α. Human hepatocellular carcinoma (HCC)-derived Huh7 cells were cultured under normoxic and hypoxic (1% O₂) conditions with or without the PKC stimulator TPA. The expression, transcriptional activity and nuclear translocation of HIF-1α were examined under treatment with PKC inhibitors, siRNAs against each PKC isoform and VK2. Hypoxia increased the expression and activity of HIF-1α. TPA increased the HIF-1α activity several times under both normoxic and hypoxic conditions. PKC-δ siRNA-mediated knockdown, PKC-δ inhibitor (rottlerin) and pan-PKC inhibitor (Ro-31-8425) suppressed the expression and transcriptional activity of HIF-1α. VK2 significantly inhibited the TPA-induced HIF-1α transcriptional activity and suppressed the expression and nuclear translocation of HIF-1α induced by TPA without altering the HIF-1α mRNA levels. These data indicate that PKC-δ enhances the HIF-1α transcriptional activity by increasing the nuclear translocation, and that VK2 might suppress the HIF-1α activation through the inhibition of PKC in HCC cells.

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PMID: 

Int J Vitam Nutr Res. 2020 Jan ;90(1-2):42-48. Epub 2019 Feb 28. PMID: 30816822

Abstract Title: 

Maximal dose-response of vitamin-K2 (menaquinone-4) on undercarboxylated osteocalcin in women with osteoporosis.

Abstract: 

Low concentrations of serum vitamin K accompany high concentrations of undercarboxylated osteocalcin (ucOC) and osteoporotic fractures. Although vitamin K2 (MK-4) is approved as a therapeutic agent for the treatment of osteoporosis in some countries, the dose-response is unknown. The objective of this study was to assess the improvement in carboxylation of osteocalcin (OC) in response to escalating doses of MK-4 supplementation. A nine-week, open-labeled, prospective cohort study was conducted in 29 postmenopausal women who suffered hip or vertebral compression fractures. Participants took low-dose MK-4 (0.5 mg) for 3 weeks (until the second visit), then medium-dose MK-4 (5 mg) for 3 weeks (until the third visit), then high-dose MK-4 (45 mg) for 3 weeks. The mean ± age of the participants was 69 ± 9 years. MK-4 dose (p 

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PMID: 

Mol Biol Rep. 2019 Dec ;46(6):5777-5783. Epub 2019 Aug 7. PMID: 31392537

Abstract Title: 

Protective effects of vitamin K2 on 6-OHDA-induced apoptosis in PC12 cells through modulation bax and caspase-3 activation.

Abstract: 

Neuroprotection using compounds with dual functions of anti-apoptotic and antioxidant effects fight against neurodegeneration. Vitamin K2 acts as a cofactor in many biochemical pathways, including sphingolipid synthesis in the nervous system, which is involved in many cellular events, including proliferation, differentiation, cellular communication, and alteration. This study aimed to investigate the protective effects of vitamin K2 in PC12 cells as an in vitro model of Parkinson's disease. The protective effects of vitamin K2 against 6-OHDA-induced apoptosis in PC12 cells were assessed using resazurin for viability, DCF-DA for ROS level, DTNB for glutathione level, flow cytometry for sub G1, and western blot analysis for detecting bax and pro-caspase-3 expression level. The results showed that 6-OHDA significantly decreased cell viability, glutathione and pro-caspase-3 levels, and increased ROS, the amount of bax in PC12 cells, while the pretreatment with 5 μM vitamin K2 significantly decreased the cell death induced by 6-OHDA. Generally, the results may present a new insight about the potential protective action of vitamin K2 against the progression of Parkinson's disease. Further studies may warrant the use of vitamin K2 as an antioxidant and anti-apoptotic agent in slowing nerve injury in neurodegenerative disease, particularly in Parkinson's disease.

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