Mangiferin alleviates ovalbumin-induced allergic rhinitis.

PMID: 

Int J Mol Sci. 2020 May 12 ;21(10). Epub 2020 May 12. PMID: 32408566

Abstract Title: 

Mangiferin Alleviates Ovalbumin-Induced Allergic Rhinitis via Nrf2/HO-1/NF-κB Signaling Pathways.

Abstract: 

Mangiferin (MF), extracted from mango trees, is considered to have anti-inflammatory, anti-apoptotic, and antioxidant effects. However, its effects on allergic rhinitis (AR), remain unclear. We investigated the mechanisms underlying the protective action of MF in ovalbumin (OVA)-induced AR models. AR was induced by OVA challenge in BALB/c mice. Prior to this, MF and dexamethasone were administered. Mice were examined for nasal mucosal inflammation, the generation of allergen-specific cytokine response, and histopathological changes in the nasal mucosa and lung tissue. MF ameliorated nasal symptoms and nasal mucosa inflammation in OVA-induced AR and reduced inflammatory cell infiltration and epithelial disruption in these tissues. MF inhibited the overproduction of Th2/Th17 cytokines and transcription factors. MF downregulated the HO-1/Nrf2 pathways, reduced oxidative stress biomarker levels, and the NF-κB signaling pathways were inhibited. MF exerts protective effects in AR by inhibiting NF-κB and activating HO-1/Nrf2 pathways. MF could be used for the treatment of AR.

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Mangiferin induces the expression of a thermogenic signature via AMPK signalling during brown-adipocyte differentiation.

PMID: 

Food Chem Toxicol. 2020 May 14:111415. Epub 2020 May 14. PMID: 32417366

Abstract Title: 

Mangiferin induces the expression of a thermogenic signature via AMPK signaling during brown-adipocyte differentiation.

Abstract: 

Mangiferin (MF) from Mangifera indica has been serendipitously found to ameliorate obesity and is used as an antioxidant, anti-inflammatory, antimicrobial, and anticancer agent. Nonetheless, the mechanism of MF-induced brown-adipose-tissue activation has not been studied. Therefore, we investigated the effect of MF on thermogenic features during brown-adipocyte differentiation. Treatment with MF improved the expression of a brown-fat signature and of mitochondrial-mass-related genes, thus resulting in UCP1 induction. MF also raised the expression of other thermogenic regulators, including peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC1α), PR domain-containing protein 16 (PRDM16), and peroxisome proliferator-activated receptors alpha and gamma (PPAR-α and -γ). MF promoted mitochondrial biogenesis, judging by increased expression of cell death-inducing DNA fragmentation factor α-like effector A (CIDEA), mitochondrial transcription factor A (TFAM), iodothyronine deiodinase 2 (DIO2), cytochrome c oxidase subunit 7A (COX7A), cyclooxygenase 2 (COX2), sirtuin 1 (SIRT1), and nuclear respiratory factor 1 (NRF1). MF treatment increased the mitochondrial DNA amount and improved mitochondrial respiratory function by increasing theoxygen consumption rate during brown-adipocyte differentiation. A gene knockdown assay involving small interfering RNA and competitive inhibition with dorsomorphin revealed that MF may promote thermogenesis in brown preadipocytes via activation of AMPK signaling. Collectively, our findings suggest that MF may be a novel pharmaceutical agent that can ameliorate obesity via activation of brown adipose tissue.

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Mangiferin is not only a remarkable anti-inflammatory compound but also an antitumor agent.

PMID: 

Environ Toxicol. 2020 May 18. Epub 2020 May 18. PMID: 32420661

Abstract Title: 

Mangiferin inhibits lipopolysaccharide-induced epithelial-mesenchymal transition (EMT) and enhances the expression of tumor suppressor gene PER1 in non-small cell lung cancer cells.

Abstract: 

Non-small cell lung cancer (NSCLC) is often complicated by pulmonary infection, which affects treatment and prognosis. Bacterial lipopolysaccharide (LPS) is an effective stimulator of inflammatory cytokine production, and previous studies have reported that LPS promotes tumor invasion and metastasis. Mangiferin is a plant-derived C-glucosylxanthone with many biological activities, such as antioxidation and anti-inflammation. This research mainly explored the mechanism of its antitumor activities on LPS-induced A549, NCI-H460, and NCI-H520 NSCLC cells. We determined that mangiferin exhibits growth inhibiting activity against LPS-induced NSCLC cells through the 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) assay. In addition, mangiferin reversed the LPS-induced downregulation of E-cadherin (epithelial marker); conversely, it significantly inhibited the expression of raised vimentin (mesenchymal markers). Moreover, the ability of NSCLC cells to migrate, as evidenced by the wound healing and transwell migration assays, and the expression of CXCR4 increased by LPS were significantly repressed by mangiferin. In addition, mangiferin markedly mediated protein levels of PER1 and NLRP3 in LPS-induced NSCLC cells and reduced the secretion of IL-1β. These results indicate that mangiferin is not only a remarkable anti-inflammatory compound but also an antitumor agent; thus, it has the potential for being developed into anti-inflammatory and antitumor drugs in the future.

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Hepatoprotective effect of meal replacement seeds juice based on sweet potato.

PMID: 

Food Sci Biotechnol. 2020 May ;29(5):693-704. Epub 2019 Nov 28. PMID: 32419968

Abstract Title: 

Hepatoprotective effect of meal replacement seeds juice based on sweet potato (MRSJ) against CCl-induced cytotoxicity in HepG2 cells.

Abstract: 

A sweet potato-based Meal Replacement Seeds Juice (MRSJ) was developed by mixing sweet potatoes and carrots with four types of seeds. Consuming the MRSJ rather than the whole vegetables or whole seeds improved digestive function, proving that it is suitable for the elderly. Its rich composition of minerals, vitamins, and unsaturated fatty acids implicates it as an excellent nutrient source. Notably, the ethyl acetate fraction of MRSJ contains abundant phenolics. The antioxidant activity assays showed that these phenolics have high radical scavenging activity, reducing power, and antioxidant capacity similar to l-ascorbic acid. The ethyl acetate fraction exerted protective effects against CCl- or HO-induced hepatotoxicity via DNA protection, lipid accumulation inhibition, and cell protection, wherein ALT and AST activities in the cell culture solution decreased significantly. These findings suggest that MRSJ consumption may protect against liver diseases. Moreover, MRSJ as an excellent nutrient source may be developed as an age-neutral food.

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Snacking on whole almonds for 6 weeks improves endothelial function and lowers LDL cholesterol.

PMID: 

Am J Clin Nutr. 2020 May 15. Epub 2020 May 15. PMID: 32412597

Abstract Title: 

Snacking on whole almonds for 6 weeks improves endothelial function and lowers LDL cholesterol but does not affect liver fat and other cardiometabolic risk factors in healthy adults: the ATTIS study, a randomized controlled trial.

Abstract: 

BACKGROUND: There is convincing evidence that daily whole almond consumption lowers blood LDL cholesterol concentrations, but effects on other cardiometabolic risk factors such as endothelial function and liver fat are still to be determined.OBJECTIVES: We aimed to investigate whether isoenergetic substitution of whole almonds for control snacks with the macronutrient profile of average snack intakes, had any impact on markers of cardiometabolic health in adults aged 30-70 y at above-average risk of cardiovascular disease (CVD).METHODS: The study was a 6-wk randomized controlled, parallel-arm trial. Following a 2-wk run-in period consuming control snacks (mini-muffins), participants consumed either whole roasted almonds (n = 51) or control snacks (n = 56), providing 20% of daily estimated energy requirements. Endothelial function (flow-mediated dilation), liver fat (MRI/magnetic resonance spectroscopy), and secondary outcomes as markers of cardiometabolic disease risk were assessed at baseline and end point.RESULTS: Almonds, compared with control, increased endothelium-dependent vasodilation (mean difference 4.1%-units of measurement; 95% CI: 2.2, 5.9), but there were no differences in liver fat between groups. Plasma LDL cholesterol concentrations decreased in the almond group relative to control (mean difference -0.25 mmol/L; 95% CI: -0.45, -0.04), but there were no group differences in triglycerides, HDL cholesterol, glucose, insulin, insulin resistance, leptin, adiponectin, resistin, liver function enzymes, fetuin-A, body composition, pancreatic fat, intramyocellular lipids, fecal SCFAs, blood pressure, or 24-h heart rate variability. However, the long-phase heart rate variability parameter, very-low-frequency power, was increased during nighttime following the almond treatment compared with control (mean difference 337 ms2; 95% CI: 12, 661), indicating greater parasympathetic regulation.CONCLUSIONS: Whole almonds consumed as snacks markedly improve endothelial function, in addition to lowering LDL cholesterol, in adults with above-average risk of CVD.This trial was registered at clinicaltrials.gov as NCT02907684.

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Whole almond consumption is associated with better diet quality and cardiovascular disease risk factors.

n/a

PMID: 

Eur J Nutr. 2020 May 16. Epub 2020 May 16. PMID: 32417945

Abstract Title: 

Whole almond consumption is associated with better diet quality and cardiovascular disease risk factors in the UK adult population: National Diet and Nutrition Survey (NDNS) 2008-2017.

Abstract: 

PURPOSE:  This work aimed to estimate whole almond consumption in a nationally representative UK survey population and examine associations with diet quality and cardiovascular disease (CVD) risk.
METHODS:  Four-day food record data from the National Diet and Nutrition Survey (NDNS) 2008-2017 (n = 6802, age ≥ 19 year) were analyzed to investigate associations between whole almond consumption and diet quality, measured by the modified Mediterranean Diet Score (MDS) and modified Healthy Diet Score (HDS), and CVD risk markers, using survey-adjusted multivariable linear regression.
RESULTS:  Whole almond consumption was reported in 7.6% of the population. Median intake in whole almond consumers was 5.0 g/day (IQR 9.3). Consumers had higher diet quality scores relative to non-consumers; higher intakes of protein, total fat, monounsaturated, n-3 and n-6 polyunsaturated fats, fiber, folate, vitamin C, vitamin E, potassium, magnesium, phosphorus, and iron; and lower intakes of trans-fatty acids, total carbohydrate, sugar, and sodium. BMI and WC were lower in whole almond consumers compared to non-consumers: 25.5 kg/m(95% CI 24.9, 26.2) vs 26.3 kg/m(25.9, 26.7), and 88.0 cm (86.2, 89.8) vs 90.1 cm (89.1, 91.2), respectively. However, there were no dose-related fully adjusted significant associations between increasing almond intake (g per 1000 kcal energy intake) and lower CVD risk markers.
CONCLUSIONS:  Almond intake is low in the UK population, but consumption was associated with better dietary quality and lower CVD risk factors. Habitual consumption of whole almonds should be encouraged as part of a healthy diet.

HIV-1-infected cell-derived exosomes promote the growth and progression of cervical cancer.

PMID: 

Int J Biol Sci. 2019 ;15(11):2438-2447. Epub 2019 Sep 7. PMID: 31595161

Abstract Title: 

HIV-1-infected cell-derived exosomes promote the growth and progression of cervical cancer.

Abstract: 

: Women infected with HIV are more likely to have aggressive cervical cancer, and patients with HIV infection are often more severely ill than those without HIV infection. However, the underlying mechanism for the progression of cervical cancer is not yet fully understood and requires further research.: Exosomes were isolated from cell culture supernatants using differential ultracentrifugation. Confirmation of exosome isolation was based upon identification by electron microscopy and NanoSight particle tracking analysis of the purified fraction. The function of exosomes derived from HIV-infected T-cells in cervical cancer was determined by CCK8 and Transwell invasion assays.: Exosomal miR-155-5p derived from HIV-infected T-cells promotes the proliferation, migration and invasion of cervical cancer cells. Furthermore, we found that HIV-infected T-cells secrete exosomal miR-155-5p that directly targets ARID2 degradation, leading to activation of the NF-κB signaling pathway. MiR-155-5p promotes cervical cancer progression by secreting proinflammatory cytokines, including IL-6 and IL-8.: In conclusion, we demonstrate that intercellular crosstalk between HIV-infected T-cells and cervical cancer is mediated by exosomes from HIV-infected T-cells that contribute to the malignant progression of cervical cancer, providing potential targets for the prevention and treatment of HIV-associated cervical cancer.

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Isolation/analysis of extracellular microvesicles from HSV-1-infected cells.

PMID: 

Methods Mol Biol. 2020 ;2060:305-317. PMID: 31617186

Abstract Title: 

Isolation/Analysis of Extracellular Microvesicles from HSV-1-Infected Cells.

Abstract: 

Extracellular vesicles (EVs) are secreted membrane vesicles, derived from endosomes or from the plasma membrane, which have been isolated from most cell types and biological fluids. Although EVs are highly heterogeneous and their classification is complex, two major categories can be distinguished: microvesicles (MVs), which derive from the shedding of the plasma membrane, and exosomes, which correspond to intraluminal vesicles released to the extracellular milieu upon fusion of multivesicular bodies (MVBs) with the plasma membrane. Cells infected with viruses may secrete MVs containing viral proteins, RNAs and, in some instances, infectious virions. A recent study carried out by our laboratory has shown that MVs released by cells infected with HSV-1 contained virions and were endocytosed by naïve cells leading to a productive infection. This suggests that HSV-1 may use MVs for spreading, expanding its tropism and evading the host immune response. Here we describe in detail the methods used to isolate and analyse the MVs released from HSV-1-infected cells.

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