PMID: 

Exp Ther Med. 2019 Jan ;17(1):551-557. Epub 2018 Nov 2. PMID: 30651835

Abstract Title: 

Eriodictyol protects H9c2 cardiomyocytes against the injury induced by hypoxia/reoxygenation by improving the dysfunction of mitochondria.

Abstract: 

Myocardial infarction is a leading cause of mortality worldwide, while myocardial ischemia and timely reperfusion contribute to myocardial injury. The mitochondria are involved in the injury and mediate the apoptosis of cardiomyocytes. In order to develop novel therapeutic approaches for myocardial infarction, the present study evaluated the myocardial protective effects of eriodictyol and investigated relevant mechanisms in H9c2 cardiomyocytes. As a result, eriodictyol was observed to improve the H9c2 cardiomyocyte viability and block the leakage of cytosolic lactate dehydrogenase under hypoxia/reoxygenation. In addition, the dysfunction of mitochondria induced by hypoxia/reoxygenation was ameliorated by eriodictyol through suppressing the overload of intracellular Ca, preventing overproduction of reactive oxygen species, blocking mitochondrial permeability transition pore opening, increasing mitochondrial membrane potential level and decreasing ATP depletion. Finally, the apoptosis of H9c2 cardiomyocyte induced by hypoxia/reoxygenation was prevented by eriodictyol through upregulation of the expression of B-cell lymphoma-2 (Bcl-2) and downregulation of the expression levels of Bcl-2-associated X protein and caspase-3. These results provided evidence for further investigation on myocardial protection and the treatment of myocardial infarction using eriodictyol.

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PMID: 

Int J Mol Sci. 2019 Mar 11 ;20(5). Epub 2019 Mar 11. PMID: 30862092

Abstract Title: 

Dietary Eriodictyol Alleviates Adiposity, Hepatic Steatosis, Insulin Resistance, and Inflammation in Diet-Induced Obese Mice.

Abstract: 

The present study aimed to investigate the molecular mechanisms underlying the anti-obesity effect of flavonoid eriodictyol (ED) supplementation in mice fed with a high-fat diet (HFD). C57BL/6N mice were fed with normal diet (ND), HFD (40 kcal% fat), or HFD + 0.005% (/) ED for 16 weeks. In HFD-induced obese mice, dietary ED supplementation significantly alleviated dyslipidemia and adiposity by downregulating the expression of lipogenesis-related genes in white adipose tissue (WAT), while enhancing fecal lipid excretion. ED additionally improved hepatic steatosis and decreased the production of pro-inflammatory cytokines by downregulating the expression of hepatic enzymes and the genes involved in lipogenesis and upregulating the expression of hepatic fatty acid oxidation-related enzymes and genes. In addition, ED improved insulin resistance (IR) by suppressing hepatic gluconeogenesis, enhancing glucose utilization, and modulating the production and release of two incretin hormones, namely gastric inhibitory polypeptide (GIP) and glucagon-like peptide-1 (GLP-1). Taken together, the current findings indicated that ED can protect against diet-induced obesity and related metabolic disturbances, including dyslipidemia, inflammation, fatty liver disease, and IR in diet-induced obese mice.

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PMID: 

J Cell Biochem. 2019 Sep ;120(9):14628-14635. Epub 2019 Apr 22. PMID: 31009103

Abstract Title: 

Eriodictyol inhibits survival and inflammatory responses and promotes apoptosis in rheumatoid arthritis fibroblast-like synoviocytes through AKT/FOXO1 signaling.

Abstract: 

2-(3,4-Dihydroxyphenyl)-5,7-dihydroxy-2,3-dihydrochromen-4-one (eriodictyol), a flavonoid compound, was proved to possess anti-inflammatory, antioxidative, and antiarthritis activities. However, the effects of eriodictyol on the rheumatoid proliferation, apoptosis, and inflammatory response of arthritis fibroblast-like synoviocytes (RA-FLS) remain unclear. Thus, the objective of this study was to examine the effects of eriodictyol on RA-FLS survival, apoptosis, and inflammatory response, and further explore the potential underlying mechanisms. Our results showed that eriodictyol inhibited the survival of RA-FLSs and promoted its apoptosis. Eriodictyol significantly reduced RA-FLS secretion of tumor necrosis factorα, interleukin 6 (IL-6), IL-8, and IL-1β. Furthermore, eriodictyol prevented the activation of the protein kinase B (AKT) pathway and increased the expression of forkhead box O1 (FOXO1) in RA-FLS. FOXO1 silence reversed the effects of eriodictyol on RA-FLS survival, apoptosis, and inflammation. Inconclusion, these findings indicated that eriodictyol inhibits the cell survival and inflammatory response in RA-FLS, and the AKT/FOXO1 signaling pathway is involved in the effect of eriodictyol on the RA-FLS. Thus, eriodictyol might be a potential therapeutic agent for the treatment of rheumatoidarthritis.

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PMID: 

Nutr Cancer. 2019 Sep 2:1-8. Epub 2019 Sep 2. PMID: 31474152

Abstract Title: 

Naringenin Suppresses Chemically Induced Skin Cancer in Two-Stage Skin Carcinogenesis Mouse Model.

Abstract: 

Naringenin, a flavonoid present in citrus fruits has many health promoting activities. It has been reported to protect skin from UV radiation, thermal damage and atopic allergies. Despite many skin protective effects,effect of naringenin on skin cancer has not been reported so far.The present work was designed to study the chemo preventive effect of naringenin on chemically induced skin cancer in mice.Two stage model of skin papillomagenesis, using DMBA plus croton oil, was used to study the effect of naringenin in Swiss albino mice. The chemo preventive effect was evaluated using morphological, histopathological and biochemical features.Oral administration of naringenin reduced the skin papilloma in both pre-treatment as well as post-treatment groups of mice. The number as well as size of papilloma was significantly reduced in the treated groups. Histopathological studies showed that naringenin treatment suppressed papillomagenesis. Biochemical studies further revealed decrease in the activity of glyoxalase-1 enzyme and an increase in carbonyl content. The effect was more pronounced in ant-initiation group.Naringenin exhibited anti-tumor effect in two stage carcinogenesis mouse skin tumor model. This study revealed that consumption of citrus fruits and the naringenin therein may be helpful in suppression of skin cancer.

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PMID: 

Molecules. 2019 Jun 25 ;24(12). Epub 2019 Jun 25. PMID: 31242703

Abstract Title: 

Essential Oil ofSuppresses Two-Stage Skin Carcinogenesis Accelerated by BRAF Inhibitor Vemurafenib.

Abstract: 

The v-raf murine sarcoma viral homolog B1 (BRAF) inhibitor drug vemurafenib (PLX4032) is used to treat melanoma; however, epidemiological evidence reveals that it could cause cutaneous keratoacanthomas and squamous cell carcinoma in cancer patients with the most prevalentmutation. In a two-stage skin carcinogenesis mouse model, the skin papillomas induced by 7,12-dimethylbenz[a]anthracene (DMBA)/12–tetradecanoylphorbol-13-acetate (TPA) (DT) resemble the lesions in BRAF inhibitor-treated patients. In this study, we investigated the bioactivity ofessential oil (KWM-EO) against PDV cells, mouse keratinocytes bearingmutation, and its effect on inhibiting papilloma formation in a two-stage skin carcinogenesis mouse model with or without PLX4032 co-treatment. Our results revealed that KWM-EO effectively attenuated cell viability, colony formation, and the invasive and migratory abilities of PDV cells. Induction of G/M cell-cycle arrest and apoptosis in PDV cells was also observed. KWM-EO treatment significantly decreased the formation of cutaneous papilloma further induced by PLX4032 in DT mice (DTP). Immunohistochemistry analyses showed overexpression of keratin14 and COX-2 in DT and DTP skin were profoundly suppressed by KWM-EO treatment. This study demonstrates that KWM-EO has chemopreventive effects against PLX4032-induced cutaneous side-effects in a DMBA/TPA-induced two-stage carcinogenesis model and will be worth further exploration for possible application in melanoma patients.

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PMID: 

Antioxidants (Basel). 2019 Aug 2 ;8(8). Epub 2019 Aug 2. PMID: 31382408

Abstract Title: 

Hepatoprotection ofL.,L. andL.

Abstract: 

The phenolic composition of hydroethanolic extracts ofL.,L. andL., obtained from plants grown under organic cultivation, was determined and their hepatoprotective effects were investigated in vitro.extract was rich in phenylethenoid glycosides, especially lavandolifolioside (254± 36 μg/mg), whereas rosmarinic acid and eriodictyol–rutinoside were the major phenolic compounds ofandextracts, accounting for 68± 7 μg/mg and 145 ± 22 μg/mg, respectively. These differential phenolic components presumably account for their dissimilar antioxidant properties. Whileextract showed moderate biological effects,extract displayed high antioxidant activity in chemical models, and that ofwas effective in counteracting potassium dichromate-induced ROS generation in human hepatocarcinoma cells. Moreover,extract (50μg/mL) and its mixture (50%/50%) withextract displayed an effective cytoprotective effect.

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PMID: 

Phytother Res. 2019 Aug 2. Epub 2019 Aug 2. PMID: 31373419

Abstract Title: 

Eriodictyol inhibits high glucose-induced extracellular matrix accumulation, oxidative stress, and inflammation in human glomerular mesangial cells.

Abstract: 

Diabetic nephropathy (DN) is one of the major complications of diabetes mellitus. The progression of DN has been found to be associated with high glucose (HG)-induced oxidative stress and inflammation in diabetes mellitus. Eriodictyol is a flavonoid that possesses antioxidant and anti-inflammatory effects. However, the effect of eriodictyol on DN remains unknown. In the present study, we evaluated the role of eriodictyol in mesangial cells (MCs) in response to HG condition. The results showed that eriodictyol repressed cell proliferation of HG-stimulated MCs. Treatment with eriodictyol attenuated oxidative stress, which was evidenced by increased superoxide dismutase activity as well as decreased production of reactive oxygen species (ROS) and malondialdehyde. Besides, eriodictyol suppressed the expressions of two NADPH oxidase (NOX) isoforms, NOX2 and NOX4, which are responsible for the generation of ROS. Eriodictyol suppressed the production of extracellular matrix proteins including fibronectin and Collagen IV, as well as the secretion of inflammatory cytokines including TNF-α, IL-1β, and IL-6 in HG-induced MCs. Moreover, the HG-induced activation of Akt/NF-κB pathway was mitigated by eriodictyol. In conclusion, eriodictyol protected MCs from HG stimulation though inhibition of Akt/NF-κB pathway.

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PMID: 

Nutrients. 2019 Jul 8 ;11(7). Epub 2019 Jul 8. PMID: 31288419

Abstract Title: 

Low-Dose Curcumin Nanoparticles Normalise Blood Pressure in Male Wistar Rats with Diet-Induced Metabolic Syndrome.

Abstract: 

Nanoparticle formulations improve bioavailability and so may allow low-dose formulations of food-derived compounds such as curcumin to attenuate chronic systemic disease despite intrinsically low oral bioavailability. The current study induced metabolic syndrome in male Wistar rats aged eight-nine weeks using a high-carbohydrate, high-fat diet (H) with corn starch diet (C) as control. Using a reversal protocol, rats were given curcumin as either nanoparticles encapsulated in poly(lactic-co-glycolic acid) (5 mg/kg/day, HCNP) or as an unformulated low dose or high-dose suspension in water (low-dose, 5 mg/kg/day, HC5; high-dose, 100 mg/kg/day, HC100) or blank nanoparticles (HBNP) for the final eight weeks of the 16 week study. We analysed cardiovascular parameters including systolic blood pressure and left ventricular diastolic stiffness along with histopathology, liver parameters including plasma liver enzymes, histopathology and metabolic parameters, including glucose tolerance, blood lipid profile and body composition, and plasma curcumin concentrations. HC100 and HCNP but not HBNP normalised systolic blood pressure (C = 120± 4; H = 143 ± 5; HBNP = 141 ± 3; HC5 = 143 ± 4; HC100 = 126 ± 4; HCNP = 128 ± 4 mmHg), left ventricular diastolic stiffness and liver fat deposition. No other improvements were induced in HC100 or HCNP or other intervention groups (HC5 and HBNP). We conclude that 5 mg/kg/day curcumin nanoparticles in H rats showed similar improvements in cardiovascular function as 100 mg/kg/day unformulated curcumin correlating with similar plasma curcumin concentrations.

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PMID: 

Cell Mol Gastroenterol Hepatol. 2019 ;7(2):457-473. Epub 2018 Sep 11. PMID: 30765332

Abstract Title: 

The Food Additive Maltodextrin Promotes Endoplasmic Reticulum Stress-Driven Mucus Depletion and Exacerbates Intestinal Inflammation.

Abstract: 

BACKGROUND & AIMS: Food additives, such as emulsifiers, stabilizers, or bulking agents, are present in the Western diet and their consumption is increasing. However, little is known about their potential effects on intestinal homeostasis. In this study we examined the effect of some of these food additives on gut inflammation.METHODS: Mice were given drinking water containing maltodextrin (MDX), propylene glycol, or animal gelatin, and then challenged with dextran sulfate sodium or indomethacin. In parallel, mice fed a MDX-enriched diet were given the endoplasmic reticulum (ER) stress inhibitor tauroursodeoxycholic acid (TUDCA). Transcriptomic analysis, real-time polymerase chain reaction, mucin-2 expression, phosphorylated p38 mitogen-activated protein (MAP) kinase quantification, and H&E staining was performed on colonic tissues. Mucosa-associated microbiota composition was characterized by 16S ribosomal RNA sequencing. For the in vitro experiments, murine intestinal crypts and the human mucus-secreting HT29-methotrexate treated cell line were stimulated with MDX in the presence or absence of TUDCA or a p38 MAP kinase inhibitor.RESULTS: Diets enriched in MDX, but not propylene glycol or animal gelatin, exacerbated intestinal inflammation in both models. Analysis of the mechanisms underlying the detrimental effect of MDX showed up-regulation of inositol requiring protein 1β, a sensor of ER stress, in goblet cells, and a reduction of mucin-2 expression with no significant change in mucosa-associated microbiota. Stimulation of murine intestinal crypts and HT29-methotrexate treated cell line cells with MDX induced inositol requiring protein 1β via a p38 MAP kinase-dependent mechanism. Treatment of mice with TUDCA prevented mucin-2 depletion and attenuated colitis in MDX-fed mice.CONCLUSIONS: MDX increases ER stress in gut epithelial cells with the downstream effect of reducing mucus production and enhancing colitis susceptibility.

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Metabolic syndrome is on the rise due to fast-food diets and inactivity, but you can fight back by adding more celery to your diet. This unassuming vegetable contains a surprising blend of antioxidants, flavonoids and other phytochemicals that work together, tackling metabolic syndrome via multiple pathways

Nature is full of powerful compounds that can boost your health, even in vegetables as unassuming as celery — and for conditions as complex and prevalent as metabolic syndrome.

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