PMID: 

Int J Environ Res Public Health. 2019 Oct 16 ;16(20). Epub 2019 Oct 16. PMID: 31623202

Abstract Title: 

Adult E-Cigarettes Use Associated with a Self-Reported Diagnosis of COPD.

Abstract: 

The use of electronic cigarettes (e-cigarettes) has increased in the US, but little is known about the effects of these products on lung health. The main purpose of this study was to examine the association between e-cigarette use and a participant's report of being diagnosed with chronic obstructive pulmonary disease (COPD) in a nationally representative sample of adults.The first wave of the Population Assessment of Tobacco and Health (PATH) survey adult data was used (= 32,320). Potential confounders between e-cigarette users and non-users were balanced using propensity score matching. Odds ratios (OR) were calculated to examine the association between e-cigarette use and COPD in the propensity-matched sample, the entire sample, different age groups, and in nonsmokers. Replicate weights and balanced repeated replication methods were utilized to account for the complex survey design.Of the 3642 participants who met the criteria for e-cigarette use, 2727 were propensity matched with 2727 non e-cigarette users. In the propensity-matched sample, e-cigarette users were more likely to report being diagnosed with COPD (OR 1.43, 95% confidence interval [CI] 1.12-1.85) than non-e-cigarette users after adjusting for confounders. The result was similar in the entire sample and in the different age subgroups. Among nonsmokers, the odds of reporting a COPD diagnosis were even greater among e-cigarette users (OR 2.94, 95% CI 1.73-4.99) compared to non-e-cigarette users.Our findings demonstrate that e-cigarette use was associated with a reported diagnosis of COPD among adults in the US. Further research is necessary to characterize the nature of this association and on the long-term effects of using e-cigarettes.

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PMID: 

Cancer Prev Res (Phila). 2019 Oct 16. Epub 2019 Oct 16. PMID: 31619443

Abstract Title: 

E-cigarettes and Cancer Risk.

Abstract: 

From the time of their introduction, the popularity of e-cigarettes (electronic nicotine delivery systems) has been rising. This trend may reflect the general belief that e-cigarettes are a less hazardous alternative to combustible cigarettes. However, the potential cancer-related effects of increased activation of the sympathoadrenal system induced by the inhalation of nicotine, the primary component of the e-cigarettes, is completely overlooked. Therefore, the aim of this review is to describe mechanisms that may connect the use of e-cigarettes and an increased risk for cancer development, as well as their stimulatory effect on cancer progression. Available pre-clinical data indicate that activation of the sympathetic nervous system by nicotine inhaled from e-cigarettes may simulate cancer development and growth by several mechanisms. This issue might be especially important for oncological patients as they may have the misconception that compared to combustible cigarettes, e-cigarettes represent a risk-free alternative.

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PMID: 

Food Funct. 2019 Oct 16 ;10(10):6655-6665. PMID: 31556890

Abstract Title: 

Maqui berry exhibited therapeutic effects against DSS-induced ulcerative colitis in C57BL/6 mice.

Abstract: 

Maqui berry (Aristotelia chilensis) is an edible berry. The study aimed to explore the therapeutic effect of maqui berry on inflammatory bowel disease. Maqui berry water extract was separated by multiple solvents extraction. The chemical bases, antioxidant and anti-inflammatory properties of different extract fractions were then compared. Dextran sodium sulfate (DSS)-induced ulcerative colitis mice were used for the pharmacological activity test in vivo. Experimental results showed that the ethyl acetate fraction of maqui berry water extract (MWE) was rich in phenols and exhibited good antioxidant and anti-inflammatory activities. MWE considerably reduced the expression of COX2 and IL-6 in LPS-stimulated RAW 264.7 cells. Inflammatory bowel disease index, MDA, NO, i-NOS, and COX2 in colon tissues and MPO, TNF-α, and IL-1β in blood serums were remarkably decreased in the treatment group compared to in the model group (p

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PMID: 

Mol Nutr Food Res. 2019 Aug 7:e1900149. Epub 2019 Aug 7. PMID: 31389663

Abstract Title: 

Protective Effects of Anthocyanins in Obesity-Associated Inflammation and Changes in Gut Microbiome.

Abstract: 

Obesity is a complex disease and a major public health epidemic. Chronic, low-grade inflammation is a common underlying feature of obesity and associated metabolic diseases; adipose tissue is a major contributor to this systemic inflammation. Evidence shows that obesity-associated inflammation may originate from gut dysfunction, including changes in intestinal bacteria or microbiome profiles. Increasingly, food and plant bioactive compounds with antioxidant and anti-inflammatory properties are proposed to ameliorate obesity-associated inflammation. Among these, the health-promoting effects of anthocyanin-rich foods are of interest here. Specifically, this review summarizes the reported benefits of anthocyanins in obesity-associated inflammation and underlying molecular mechanisms, including the role of gut microbiome and cell signaling pathways regulated by anthocyanins both in vivo and in vitro.

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PMID: 

J Nutr Sci Vitaminol (Tokyo). 2019 ;65(Supplement):S59-S61. PMID: 31619648

Abstract Title: 

Myo-Inositol for the Prevention of Gestational Diabetes Mellitus. A Brief Review.

Abstract: 

Gestational Diabetes Mellitus (GDM) is one of the most frequent complications of pregnancy and is characterized by a carbohydrate intolerance which is diagnosed with the oral glucose tolerance test. The prevalence of GDM in our population is about 12%, but risk factors like a previous GDM, ethnicity, a parent with diabetes mellitus type 2 and maternal overweight may increase its occurrence. Complications of GDM are a pre-term birth (before 37 wk gestation), macrosomia (birth weight≥4 kg) and gestational hypertension. Actually, GDM is principally treated with diet and, if it is necessary, with insulin; but the challenge is the prevention of GDM. Among the measures used, changes in life-style (diet+exercise) failed to prevent GDM whereas metformin showed conflicting results.A promising supplement is myo-inositol (MI) which was given from first trimester until delivery to women at risk for GDM reporting a significant decrease in GDM occurrence by more than 60% comparing to the placebo group. Recently, a secondary analysis from 3 randomized controlled trials demonstratedthat MI may also significantly reduce some of GDM complications such as pre-term birth and macrosomia with a favorable impact on mother and fetus well being.

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PMID: 

Nan Fang Yi Ke Da Xue Xue Bao. 2018 Nov 30 ;38(11):1378-1383. PMID: 30514689

Abstract Title: 

[Combined treatment with myo-inositol and luteolin selectively suppresses growth of human lung cancer A549 cells possibly by suppressing activation of PDK1 and Akt].

Abstract: 

OBJECTIVE: To study the effects of myo-inositol and luteolin on human lung cancer A549 cells and explore the possible mechanisms.METHODS: A549 cells were treated with different concentrations of myo-inositol and luteolin, either alone or in combination, and the cell viability was examined using MTT assay. A549 cells and human bronchial epithelial Beas-2B cells were treated for 48 h with 10 mmol/L myo-inositol and 20μmol/L luteolin, alone or in combination, and the cell proliferation was detected using MTT assay; the colony formation and migration of the cells were examined with colony formation assay and wound healing assay, respectively. The protein expression levels in A549 cells were detected using Westernblotting.RESULTS: Both myo-inositol and luteolin could dose-dependently inhibit the viability of A549 cells. Treatments with 10 mmol/L myo-inositol, 20μmol/L luteolin, and both for 48 h caused significant reduction in the cell viability (92%, 83% and 70% of the control level, respectively) and colony number (79%, 73% and 43%, respectively), and significantly lowered the wound closure rate (24.61%, 13.08% and 8.65%, respectively, as compared with29.99% in the control group). Similar treatments with myoinositol and luteolin alone or in combination produced no significant inhibitory effect on the growth, colony formation or migration of Beas-2B cells. The expressions of p-PDK1 and p-Akt in myo-inositol-treated A549 cells and the expression ofpPDK1 in luteolin-treated cells were significantly decreased (< 0.05), and the decrements were more obvious in the combined treatment group (< 0.05).CONCLUSIONS: Luteolin combined with myo-inositol can selectively inhibit the proliferation and migration of A549 cells, and these effects are probably mediated, at least in part, by suppressing the activation of PDK1 and Akt.

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PMID: 

Zhongguo Shi Yan Xue Ye Xue Za Zhi. 2018 Oct ;26(5):1425-1429. PMID: 30295262

Abstract Title: 

[Effects of Luteolin on Proliferation and Programmed Cell Death of Human Multiple Myeloma Cell RPMI-8226].

Abstract: 

OBJECTIVE: To investigate the effect of Luteolin on proliferation and cell death of human multiple myeloma cell line RPMI-8226 and its mechanisms.METHODS: The effect of Luteolin on the growth of human multiple myeloma cell line RPMI-8226 was detected by CCK-8, and then the minimal effective concentration was determined and was used to treat RPMI-8226 cells. The effects of luteolin and chloroquine on expression of cleaved-caspase 3 and LC3 in RPMI8826 cells was detected by Western blot.RESULTS: The luteolin significant inhibited RPMI-8226 cell proliferation in a dose-dependent manner. Treatment with lutedin 40-80µmol/L for 24 hours and luteolin 20-80µmol/L for 48 hours inhibited RPMI-8226 cell proliferation in a dose-dependent manner (24 h, r= -0.983; 48 h, r= -0.985). After treatment with lutelin 20µmol/L for 48 h, the expression of cleaved caspase3 and LC3 Ⅱ/Ⅰ in RPMI 8826 cells significantly increased; after treatment with chloroquine at the same time, the expression of cleaved-caspase 3 and LC3 Ⅱ/Ⅰ significantly decreased.CONCLUSION: Luteolin inhibits the proliferation of RPMI-8226 cells by inducing the pathways of both apoptosis and autophagy, moreover the actions of apoptosis and autophagy are interactive or/and promotive each other.

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PMID: 

J Cancer. 2018 ;9(20):3669-3675. Epub 2018 Sep 8. PMID: 30405835

Abstract Title: 

Luteolin exerts an anticancer effect on gastric cancer cells through multiple signaling pathways and regulating miRNAs.

Abstract: 

Accumulating studies confirmed that luteolin, a common dietary flavonoid which is widely distributed in plants and has diverse beneficial biological function, including anti-oxidant, anti-inflammation and anticancer properties. However, the detail mechanisms of luteolin on GC are poorly understood. Here, we investigated the anticancer effect of luteolin in GC cellsand. Luteolin reduced the cell viability in a time and dose-dependent manner. Luteolin significantly inhibited cell cycle progress, colony formation, proliferation, migration, invasion and promoted apoptosisand. Luteolin also regulated these biological effects associated regulators. Mechanically, luteolin treatment regulated Notch1, PI3K, AKT, mTOR, ERK, STAT3 and P38 signaling pathways and modulated a series of miRNAs expression. These findings provide novel insight into the molecular function of luteolin which suggest its potential as a therapeutic agent for human GC.

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PMID: 

Neurosci Lett. 2019 01 23 ;692:90-99. Epub 2018 Oct 26. PMID: 30420334

Abstract Title: 

Therapeutic potential of luteolin in transgenic Drosophila model of Alzheimer's disease.

Abstract: 

A transgenic fly line expressing wild type human Aβ42 were exposed to luteolin mixed in diet at final concentration of 5, 10, 15 and 20μM. The climbing assay, activity pattern, life span, aversive phototaxis suppression assay (APS) along with the estimation of protein carbonyl content (PCC), glutathione-S-transferase (GSTs) activity, glutathione(GSH) content, lipid peroxidation (LPO), acetylcholinesterase activity (AChE), superoxide dismutase (SOD) activity, catalase (CAT) activity, caspase 3 and 9 activities in the brain of treated as well as untreated AD flies (Positive control) were studied. Histopathology of Drosophila brain sections was done by performing thioflavin-S, Bielschowsky's silver staining and toluidine blue staining. A dose-dependent increase in the life span, delay in the loss of climbing ability as well as activity was observed in AD flies exposed to luteolin compared to unexposed AD flies. A dose-dependent reduction in LPO, PCC, GST, AChE, SOD, CAT, caspase 9 and caspase 3 activity and an increase in the GSH content was also observed. Histopathological examination of fly brains using thioflavin-S and silver staining has revealed a significant dose-dependent reduction in the expression of Aβ42 peptides in ADfly groups exposed to 10, 15 and 20μM of luteolin. No gross morphological changes were observed in the brain sections of AD and control flies stained with toluidine blue. Molecular docking results have revealed that luteolin binds to AChE and Aβ42 at specific sites that might result in the inhibition of AChE and disaggregation/prevention of Aβ42 plaque formation.

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PMID: 

Int J Oncol. 2019 Feb ;54(2):665-672. Epub 2018 Nov 14. PMID: 30431076

Abstract Title: 

Luteolin sensitizes human liver cancer cells to TRAIL‑induced apoptosis via autophagy and JNK‑mediated death receptor 5 upregulation.

Abstract: 

The tumor necrosis factor‑related apoptosis‑inducing ligand (TRAIL) is a dynamic cytokine that initiates the apoptosis of cancer cells, but exhibits little or no toxicity in normal cells. Luteolin is a flavonoid compound frequently used in the treatment of cancer. In the current study, we demonstrate that treatment with luteolin and TRAIL exerts a synergistic effect and the mechanisms on TRAIL‑resistant Huh7 cells. The results demonstrated that luteolin induced an autophagic flux in human liver cancer cells. The attenuation of the autophagic flux by applying the specific inhibitor of autophagy, chloroquine, significantly suppressed DR5 expression. Treatment with genetically modified autophagy‑related 5 siRNA abrogated the luteolin‑mediated sensitizing effect of TRAIL. Furthermore, pre‑treatment with the c‑Jun N‑terminal kinase (JNK) inhibitor, SP600125, significantly attenuated the luteolin‑induced upregulation of DR5 expression, thereby suggesting that JNK activation promotes DR5 expression. Our findings also revealed that Akt phosphorylation was required for TRAIL sensitization. On the whole, the findings of this study indicated that luteolin effectively enhanced TRAIL‑initiated apoptosis, and that these effects were likely to be mediated by autophagy and JNK‑mediated DR5 expression.

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