Ping Yao

Huazhong University of Science and Technology, Wu-han-shih, Hubei, China

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Publications (84)254.8 Total impact

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    ABSTRACT: Although the association of Helicobacter pylori (H. pylori) infection with diabetes mellitus has been evaluated, findings are controversial. This study investigated the association in a Chinese population. A cross-sectional study, including a total of 30,810 subjects from the Dongfeng-Tongji Cohort study was conducted. H. pylori status was measured via (14) C urea breath test. Association analysis was performed by logistic regression, with multivariable adjustment for sex, age, BMI, smoking, alcohol consumption, family history of diabetes, physical activity, and the use of antibiotics. Among a middle- and old-age Chinese population, Individuals with H. pylori infection also had a higher prevalence of type 2 diabetes (21.3% vs.20.2%, P = 0.026). H. pylori infection was associated with higher risk of type 2 diabetes (OR, 1.08 [95% CI: 1.02-1.14]; P = 0.008) after adjustment for other confounders. The association was significant among females, those who were above 65 years old, not overweight or obese, and those who did not smoke, did not consume alcohol and without family history of diabetes. However, there was no interaction between H. pylori infection and other traditional risk factors on type 2 diabetes risk. Subjects with H. pylori infection had a lower level of HDL cholesterol (P < 0.0001) and higher levels of blood pressure (P < 0.001), total cholesterol, HbA1c and fasting blood glucose (P < 0.0001) than those who did not. These findings suggested that H. pylori infection was associated with the risk of type 2 diabetes in a middle- and old-age Chinese population. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Diabetes/Metabolism Research and Reviews 07/2015; DOI:10.1002/dmrr.2677 · 3.59 Impact Factor
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    ABSTRACT: Hypoxia is a prominent characteristic of inflammatory tissue lesions. It can affect platelet function. While mean platelet volume (MPV) and platelet distribution width (PDW) are sample platelet indices, they may reflect subcinical platelet activation. To investigated associations between adiposity indices and platelet indices, 17327 eligible individuals (7677 males and 9650 females) from the Dongfeng-Tongji Cohort Study (DFTJ-Cohort Study, n=27009) were included in this study, except for 9682 individuals with missing data on demographical, lifestyle, physical indicators and diseases relative to PDW and MPV. Associations between adiposity indices including waist circumstance (WC), waist-to-height ratio (WHtR), body mass index (BMI), and MPV or PDW in the participants were analyzed using multiple logistic regressions. There were significantly negative associations between abnormal PDW and WC or WHtR for both sexes (ptrend<0.001 for all), as well as abnormal MPV and WC or WHtR among female participants (ptrend<0.05 for all). In the highest BMI groups, only females with low MPV or PDW were at greater risk for having low MPV (OR=1.33, 95% CI=1.10, 1.62 ptrend<0.001) or PDW (OR=1.34, 95% CI=1.14, 1.58, ptrend<0.001) than those who had low MPV or PDW in the corresponding lowest BMI group. The change of PDW seems more sensitive than MPV to oxidative stress and hypoxia. Associations between reduced PDW and MPV values and WC, WHtR and BMI values in Chinese female adults may help us to further investigate early changes in human body.
    PLoS ONE 06/2015; 10(6):e0129677. DOI:10.1371/journal.pone.0129677 · 3.53 Impact Factor
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    ABSTRACT: Pu-erh tea is a special post-fermented tea product that contains various compounds. Quinocetone (QCT) has been used as a veterinary drug in P.R. China. However, QCT has been proven to cause oxidative DNA damage, inflammation, and apoptosis. We have used Pu-erh black tea extract (BTE) as an intervention for QCT-treated SD rats and analyzed its protective effect. Our data demonstrated that BTE improved QCT-induced functional and organic liver damage. This protective effect was accomplished by activating the Nrf2/HO-1 pathway expression and the potential mechanism consisted in the activation of the extracellular signal-regulated kinase (ERK) pathway by polyphenols contained in BTE. Moreover, some flavonoids and quinone (also contained in BTE) might effectively activate Nrf2/HO-1 pathway expression and protect SD rats from oxidative stress. Thus, the protective effect of BTE against QCT-induced oxidative damage demonstrated new insights into the antioxidative mechanisms of Pu-erh tea.
    Journal of Functional Foods 04/2015; 14:767-778. DOI:10.1016/j.jff.2015.03.004 · 4.48 Impact Factor
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    ABSTRACT: Background/Aims: Curcuminoids are the main bioactive constituents of the rhizome of turmeric. Erythrocytes lesions in diabetes are probably related to hyperglycemia and protein glycation. It has been reported that curcumin prevent lipid peroxidation. However, reports on the effects of demethoxycurcumin and bis-demethoxycurcumin on human erythrocytes at high glucose levels are scarce. Our aim is to investigate the effect of curcuminoids on oxidative stress and membrane of erythrocytes exposed to hyperglycemic condition. Methods: In this study, the different blood samples were treated with two doses of glucose (10 or 30 mM) to mimic hyperglycemia in the presence or absence of three kinds of curcuminoids (5 or 10 μM) in a medium at 37 °C for 24 h (Each experiment consists of 20 blood samples from 10 male and 10 female volunteers). The malondialdehyde was checked by HPLC, antioxidase (GSH and GSSG) were measured by LC/MS, SOD was checked by WST-1 kit, morphology and phospholipid symmetry were detected by flow cytometry, confocal scanning microscope and scanning electron microscope. Results: The results illustrated that all three curcuminoids reduce oxidative stress damage on the membrane and maintain a better profile for erythrocytes. Furthermore, three curcuminoids had benefit effects on antioxidase. Conclusion: The three kinds of curcuminoids supplementation may prevent lipid peroxidation at different intensity and membrane dysfunction of human erythrocytes in hyperglycemia.
    Cellular Physiology and Biochemistry 01/2015; 2015(35):789-802. DOI:10.1159/000369738 · 3.55 Impact Factor
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    ABSTRACT: The prevalence of metabolic syndrome (MetS) persistently increased. Several studies have found serum creatinine (SCr) concentrations related to cardiovascular disease and type 2 diabetes. The relationship between SCr concentrations and MetS are unknown. We measured SCr concentrations and MetS in 22363 individuals (10,151 males, 12,212 females) from the Dongfeng-Tongji Cohort in Shiyan, China from 2008 to 2009. The prevalence of MetS was 30.6% in the study population. In the multivariable-adjusted logistic regression analyses, higher SCr concentrations were associated with a higher risk of MetS (P trend<0.0001). Compared with the lowest extreme quintiles, subjects with the highest quintiles had 1.34 fold risk of MetS (95% confidence interval (CI): 1.22-1.47). The SCr concentrations were also associated with the individual component of MetS. In addition, higher SCr concentrations were associated with higher risk of MetS with more components. There is a graded positive association between the SCr concentrations and MetS risk in a middle aged and older Chinese population. Higher SCr concentrations, even within normal ranges, were associated with higher risk of MetS. The SCr might be a useful indicator of MetS and its related diseases. Copyright © 2014. Published by Elsevier B.V.
    Clinica Chimica Acta 12/2014; 440. DOI:10.1016/j.cca.2014.11.025 · 2.82 Impact Factor
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    ABSTRACT: To investigate the effect of passive smoking on the changes in mean platelet volume (MPV) in healthy adults. Participants (N = 17,825) were drawn from the Dongfeng-Tongji cohort. Multiple logistic regression analysis was used to examine relationships between MPV and selected variables among subgroups of MPV clarified by the MPV reference range for Chinese adults. Female never smokers exposed to passive smoke ≥ 60 minutes every day (OR: 1.471, 95%CI: 1.147-1.886) or ≥ 30 years had a higher risk of having low MPV (OR: 1.260, 95%CI: 1.004-1.583). Certain duration of passive smoke exposure (≥ 60 minutes/day or ≥ 30 years) was associated with higher risk of having low MPV in female never smokers.
    American journal of health behavior 07/2014; 38(4):519-28. DOI:10.5993/AJHB.38.4.5 · 1.31 Impact Factor
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    ABSTRACT: Objective Emerging evidence has demonstrated that chronic ethanol exposure induces iron overload, enhancing ethanol-mediated liver damage. The purpose of this study was to explore the effects of the naturally-occurring compound quercetin on ethanol-induced iron overload and liver damage, focusing on the signaling pathway of the iron regulatory hormone hepcidin. Methods and Results Adult male C57BL/6J mice were pair-fed with isocaloric-Lieber De Carli diets containing ethanol (accounting for 30% of total calories) and/or carbonyl iron (0.2%) and treated with quecertin (100 mg/kg body weight) for 15 weeks. Mouse primary hepatocytes were incubated with ethanol (100 mM) and quercetin (100 μM) for 24 hours. Mice exposed to either ethanol or iron presented significant fatty infiltration and iron deposition in the liver; these symptoms were exacerbated in mice co-treated with ethanol and iron. Quercetin attenuated the abnormity induced by ethanol and/or iron. Ethanol suppressed BMP6 and intranuclear SMAD4 as well as decreased hepcidin expression. These effects were partially alleviated by quercetin supplementation in mice and hepatocytes. Importantly, ethanol caused suppression of SMAD4 binding to the HAMP promoter and of hepcidin mRNA expression. These effects were exacerbated by anti-BMP6 antibody and partially alleviated by quercetin or human recombinant BMP6 in cultured hepatocytes. In contrast, co-treatment with iron and ethanol, especially exposure of iron alone, activated BMP6/SMAD4 pathway and up-regulated hepcidin expression, which was also normalized by quercetin in vivo. Conclusions Quercetin prevented ethanol-induced hepatic iron overload different from what carbonyl iron diet-elicited in the mechanism, by regulating hepcidin expression via the BMP6/SMAD4 signaling pathway.
    The Journal of nutritional biochemistry 06/2014; DOI:10.1016/j.jnutbio.2014.02.009 · 4.59 Impact Factor
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    ABSTRACT: Leucine, a branched-chain amino acid, has been shown to promote glucose uptake and increase insulin sensitivity in skeletal muscle, but the exact mechanism remains unestablished. We addressed this issue in cultured skeletal muscle cells in this study. Our results showed that leucine alone did not have an effect on glucose uptake or phosphorylation of protein kinase B (AKT), but facilitated the insulin-induced glucose uptake and AKT phosphorylation. The insulin-stimulated glucose uptake and AKT phosphorylation were inhibited by the phosphatidylinositol 3-kinase inhibitor, wortmannin, but the inhibition was partially reversed by leucine. The inhibitor of mammalian target of rapamycin complex 1 (mTORC1), rapamycin, had no effect on the insulin-stimulated glucose uptake, but eliminated the facilitating effect of leucine in the insulin-stimulated glucose uptake and AKT phosphorylation. In addition, leucine facilitation of the insulin-induced AKT phosphorylation was neutralized by knocking down the core component of the mammalian target of rapamycin complex 2 (mTORC2) with specific siRNA. Together, these findings show that leucine can facilitate the insulin-induced insulin signaling and glucose uptake in skeletal muscle cells through both mTORC1 and mTORC2, implicating the potential importance of this amino acid in glucose homeostasis and providing new mechanistic insights.
    Amino Acids 05/2014; 46(8). DOI:10.1007/s00726-014-1752-9 · 3.65 Impact Factor
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    ABSTRACT: Quinocetone (3-methyl-2-quinoxalin benzenevinylketo-1, 4-dioxide, QCT) is a widely used veterinary drug in P.R. China that promotes feed efficiency and growth of various animals. However, its potential toxicity has been concerned recently. In the present study, we investigated QCT-induced hepatocyte changes and its related mechanism, especially the expression of Nrf2/HO-1 pathway. Oxidative stress induced by QCT in hepatocyte led to DNA damage, inflammation and apoptosis. Nevertheless, hepatocyte has a self-repair system to protect itself from oxidative stress. In the 50 mg/kg/day QCT group, the morphology and function of liver were approximately maintained on normal level, which indicated that the damaged cell might have a self-repair mechanism. Notably, nuclear factor-erythroid 2-related factor 2/heme oxygenase-1 (Nrf2/HO-1) pathway plays a critical role in protecting cells against reactive oxygen species (ROS) generation. However, higher doses of QCT (800 mg/kg/day and 2400 mg/kg/day) inhibited the expression of Nrf2/HO-1 pathway, which resulted in excessive ROS generation and irreversible oxidative DNA damage, inflammation and apoptosis. In conclusion, although QCT-induced oxidative stress activates the expression of Nrf2/HO-1 pathway initially, persistent QCT exposure will inhibit this expression and aggravate hepatocyte damage. Simultaneously, inflammation and apoptosis continues to progress, liver dysfunction and tissue damage will be occurred eventually.
    Food and chemical toxicology: an international journal published for the British Industrial Biological Research Association 04/2014; 69. DOI:10.1016/j.fct.2014.04.026 · 2.61 Impact Factor
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    ABSTRACT: Emerging evidence has displayed that oxygen free radicals especially ones promoted by "free" iron play an important role in the development of alcoholic liver disease (ALD). Naturally-occurring quercetin has been reported to prevent ALD and iron overload-induced damage aside from the "free" iron. The purpose was to explore the potential mechanisms by which quercetin arrests alcohol-induced "free" iron disorder. Chronic alcohol (30% of total calories) or iron (0.2%)-fed adult male C57BL/J mice for 15 weeks resulted in significantly elevated levels of hepatic iron, labile iron pool-Fe and serum non-transferrin bound iron, accompanied with sustained oxidative damage. The hepatotoxicity was further exacerbated by ethanol and iron. Quercetin (100 mg/kg. body weight) alleviated the detrimental effects induced by ethanol and/or iron. The expressions of divalent metal transporter 1, zinc transporter member 14, mucolipin 1, transferrin receptor 1 (TfR1) and ferritin were up-regulated by ethanol and/or iron, which were partially normalized by quercetin. Quercetin prevented ethanol-induced hepatotoxicity, which may be partially attributed to the alleviated disorder of bound iron and "free" iron. The significant suppression of ethanol-stimulated molecules for "free" iron uptake and release may contribute to the hepatoprotective effect of quercetin, although TfR1-mediated physiological pathway of iron uptake also played a role.
    Food and chemical toxicology: an international journal published for the British Industrial Biological Research Association 02/2014; 67. DOI:10.1016/j.fct.2014.02.022 · 2.61 Impact Factor
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    ABSTRACT: Quinocetone (3-methyl-2-quinoxalin benzenevinylketo-1,4-dioxide, QCT) is a widely used veterinary drug in PR China that promotes feed efficiency and growth of various animals. However, its potential toxicity has been concerned recently. In the present study, we investigated QCT-induced hepatocyte changes and its related mechanism, especially the expression of Nrf2/HO-1 pathway. Oxidative stress induced by QCT in hepatocyte led to DNA damage, inflammation and apoptosis. Nevertheless, hepatocyte has a self-repair system to protect itself from oxidative stress. In the 50 mg/kg/day QCT group, the morphology and function of liver were approximately maintained on normal level, which indicated that the damaged cell might have a self-repair mechanism. Notably, nuclear factor-erythroid 2-related factor 2/heme oxygenase-1 (Nrf2/HO-1) pathway plays a critical role in protecting cells against reactive oxygen species (ROS) generation. However, higher doses of QCT (800 mg/kg/day and 2400 mg/kg/day) inhibited the expression of Nrf2/HO-1 pathway, which resulted in excessive ROS generation and irreversible oxidative DNA damage, inflammation and apoptosis. In conclusion, although QCT-induced oxidative stress activates the expression of Nrf2/HO-1 pathway initially, persistent QCT exposure will inhibit this expression and aggravate hepatocyte damage. Simultaneously, inflammation and apoptosis continues to progress, liver dysfunction and tissue damage will be occurred eventually.
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    ABSTRACT: Oxidative stress plays a pivotal role in the intense exercise-induced myocardium injury, and mitochondrial compartment is presumed as the main source and susceptible target of intracellular reactive oxygen species (ROS). The objective of this study was to evaluate the protective effect of quercetin, a naturally occurring flavonoids possessing antioxidant effect on repeated intense exercise-induced mitochondrial oxidative stress and dysfunction. Adult male BALB/C mice were treated by quercetin (100 mg/kg bw) for 4 weeks and subjected to the exercise protocol on a treadmill (28 m/min at 5° slope for 90 min) for seven consecutive days concurrently at the fourth week. Intense exercise in mice resulted in the leakage of creatine kinase-MB (increased from 221.5 ± 33.8 to 151.1 ± 19.1 U/l, P < 0.01) and ultrastructural malformation mainly evidenced by disrupted myofibrils and swollen mitochondria, which was overtly attenuated by quercetin prophylaxis. Quercetin pretreatment evidently alleviated mitochondrial oxidative stress by inhibiting glutathione depletion and aconitase inactivation, ROS over-generation, and lipid peroxidation in cardiac mitochondria of intense exercise mice. Furthermore, mitochondrial dysfunction manifested by decreased mitochondrial membrane potential (68.6 ± 7.6 versus 100.0 ± 7.7 %, P < 0.01) and respiratory control ratio (5.03 ± 0.55 versus 7.48 ± 0.71, P < 0.01) induced as a consequence of acute exercise was markedly mitigated by quercetin precondition. Quercetin protects mouse myocardium against intense exercise injury, especially ultrastructural damage and mitochondrial dysfunction, probably through its beneficial antioxidative effect, highlighting a promising strategy for over-training injury by naturally occurring phytochemicals.
    Arbeitsphysiologie 12/2013; 114(4). DOI:10.1007/s00421-013-2802-9 · 2.30 Impact Factor
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    ABSTRACT: Deoxynivalenol (DON) is one of the most common mycotoxins. The aim of this study consists in using diverse cellular and molecular assays to evaluate cytotoxicity, genotoxicity as well as oxidative damage and to investigate their mechanisms in human peripheral blood lymphocytes. The human lymphocytes were cultured in eight different doses of DON (0, 6.25, 12.5, 25, 50, 100, 250 and 500 ng/mL) during 6; 12; and 24 h. DON was able to decrease cell viability and cause damage to the membrane, the chromosomes or the DNA at all times of culture. It was also able to induce lipid peroxidation and raise the levels of 8-OHdG and ROS in 6, 12 and 24 h. The results of the RT-PCR and the Western Blot indicated that DON is able to enhance mRNA or protein expressions of DNA repair genes and HO-1 in 6 h and to inhibit these expressions in 24 h. DON potentially triggers genotoxicity in human lymphocytes. This mechanism is probably related to depletion of antioxidase and oxidative damage to the DNA that reduced expression of HO-1, thereby inhibiting the ability of DNA repair.
    Food and chemical toxicology: an international journal published for the British Industrial Biological Research Association 12/2013; 64. DOI:10.1016/j.fct.2013.12.012 · 2.61 Impact Factor
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    ABSTRACT: Though both SLC30A8 rs13266634 SNP and plasma zinc concentrations have been associated with impaired glucose regulation (IGR) and type 2 diabetes (T2D), their interactions for IGR and T2D remain unclear. Therefore, to assess zinc-SLC30A8 interactions, we performed a case-control study in 1,796 participants: 218 newly diagnosed IGR patients, 785 newly diagnosed T2D patients, and 793 individuals with normal glucose tolerance (NGT). After adjustment for age, sex, BMI, family history of diabetes and hypertension, the multivariable OR of T2D associated with a 10-µg/dl higher plasma zinc level was 0.87 (0.85-0.90). Meanwhile, the OR of SLC30A8 rs13266634 homozygous genotypes CC compared with TT was 1.53 (1.11-2.09) for T2D. Similar associations were found in IGR and IGR&T2D groups. Each 10-µg/dl increment of plasma zinc was associated with 22% (OR, 0.78; 95% CI, 0.72-0.85) lower odds of T2D in TT genotype carriers, 17% (0.83; 0.80-0.87) lower odds in CT genotype carriers, and 7% (0.93; 0.90-0.97) lower odds in CC genotype carriers (P for interaction = 0.01). Our study suggested that the C allele of rs13266634 was associated with higher odds of T2D, and higher plasma zinc was associated with lower odds. The inverse association of plasma zinc concentrations with T2D was modified by SLC30A8 rs13266634. Further studies are warranted to confirm our findings and clarify the mechanisms underlying the interaction between plasma zinc and the SLC30A8 gene in relation to T2D.
    Diabetes 12/2013; 63(5). DOI:10.2337/db13-0606 · 8.47 Impact Factor
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    ABSTRACT: High carbohydrate antigen 125 (CA-125) level was reported to be associated with some cardiac dysfunctions, such as chronic heart failure, but the relationship between CA-125 level and coronary heart disease (CHD) risk remains unclear. The aim of this study was to explore the potential association in a Chinese older population. In a population-based case-control study conducted in a Chinese older population, serum CA-125 levels were measured in 1177 diagnosed CHD patients and 3531 age and sex matched control subjects without CHD. Serum CA-125 level was significantly higher in CHD patients than controls (P < 0.001) with adjustment for age, gender, smoking, drinking, BMI, physical activity, hypertension, dyslipidemia, diabetes mellitus, medication history and family history of CHD and myocardial infarction. CHD risk was doubled (OR: 2.10, 95%CI: 1.69-2.60) among subjects in the highest quartile compared to those in the lowest quartile of CA-125 level (P trend < 0.001). Furthermore, CA-125 levels were associated with CHD risks in subjects with age over 60 years (OR: 2.19, 95%CI: 1.75-2.73), current smokers (OR: 2.29, 95%CI: 1.50-3.49), current drinkers (OR: 2.35, 95%CI: 1.57-3.53) and subjects with hypertension (OR: 2.04, 95%CI: 1.71-2.43). Elevated serum CA-125 level might be associated with increased risk of coronary heart disease in the Chinese older population. Further investigations are needed to identify the possible biological role of CA-125 in CHD development in the future.
    PLoS ONE 11/2013; 8(11):e81328. DOI:10.1371/journal.pone.0081328 · 3.53 Impact Factor
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    ABSTRACT: Nanobiotechnology has been recently viewed as a promising strategy to improve therapy efficacy by promoting the accumulation of hydrophobic bioactive compounds in tissues. The aim of present study was to formulate a novel quercetin-loaded cationic nanostructured lipid carriers (QR-CNLC) and to evaluate its biodistribution in vivo after oral administration. QR-CNLC were prepared by emulsifying at high temperature and subsequent solidifying at low temperature using various functional ingredients, and its characteristics, including physical index, release profile in vitro, and tissue distribution in vivo, were investigated. The results demonstrated that QR-CNLC exhibited an average particle size 126.6nm, a zeta potential of 40.5mV and 89.3% entrapment efficiency. QR-CNLC performed slower release compared with quercetin solution in vitro. QR-CNLC showed higher AUC (area under tissue concentration-time curve) value and higher Cmax value in lung, liver and kidney compared with control group. The value of relative intake rate (re) for lung, liver and kidney was 1.57, 1.51 and 1.68, respectively, which revealed that quercetin can be significantly accumulated in lung, kidney and liver after oral administration of QR-CNLC compared with quercetin suspension. In conclusion, cationic nanostructured lipid carriers may be an attractive nanocarrier system for oral delivery of hydrophobic functional components.
    Colloids and surfaces B: Biointerfaces 11/2013; 115C:125-131. DOI:10.1016/j.colsurfb.2013.11.029 · 4.29 Impact Factor
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    ABSTRACT: To investigate the possible molecular mechanisms of heme oxygenase-1 (HO-1) induction by quercetin using rat primary hepatocytes. Sprague-Dawley rat primary hepatocytes were isolated using a two-step collagenase perfusion technique and treated with quercetin at various doses (25 - 200 mumol/L) and times (2 - 12 h). To investigate the roles of various signaling pathways, the hepatocytes were pre-treated with 50 mumol/L quercetin plus an extracellular signal-regulated kinase (ERK) inhibitor (PD98059 at 10 mumol/L), a p38 inhibitor (SB203580 at 10 mumol/L), a c-Jun N-terminal kinase inhibitor (SP600125 at 10 mumol/L) or a phosphatidylinositol 3-kinase inhibitor (Wortmannin at 1 mumol/L) for 12 h. Changes in the mRNA and protein levels of HO-1 and nuclear factor, ethryroid-2 related factor 2 (Nrf2) were detected by RT-PCR and western blotting. After 4 - 12 h of treatment with quercetin at all concentrations, the HO-1 mRNA level in hepatocytes had increased significantly (vs. untreated control cells; all P less than 0.01). The quercetin-induced HO-1 expression and Nrf2 translocation into the nucleolus was inhibited by PD98059. Quercetin may induce HO-1 expression via the ERK/Nrf2 signaling transduction pathway.
    Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology 11/2013; 21(11):865-868.
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    ABSTRACT: MicroRNAs (miRNAs), a class of small non-coding RNAs, are thought to serve as crucial regulators of gene expression. Dysregulated expression of miRNAs has been described in various diseases and may contribute to related pathologic processes. Our aim was to examine circulating miRNA-146a levels in newly diagnosed type 2 diabetes mellitus (new-T2DM) patients from a Chinese Han population. Circulating miRNA-146a was extracted from plasma samples of 90 new-T2DM patients and 90 age- and sex-matched controls. Quantitative PCR assessment revealed that circulating miRNA-146a levels were significantly elevated in new-T2DM patients compared with controls. Participants in the highest tertile of circulating miRNA-146a levels showed a notably higher risk for new-T2DM (crude OR 4.333, 95% CI, 1.935 to 9.705, P = 0.001) than persons in the lowest tertile. Controlling for known risk factors and some biochemical indicators did not attenuate the aforementioned association. In addition, receiver operating characteristic (ROC) curves generated for miRNA-146a revealed an area under the curve (AUC) of 0.725 (95% CI, 0.651 to 0.799, P < 0.001). Moreover, higher circulating miRNA-146a levels were significantly associated with higher plasma heme oxygenase-1 (HO-1) concentrations (β coefficient = 0.131, P < 0.001) and lower HOMA-beta (β coefficient = -0.153, P = 0.015). We found that circulating miRNA-146a levels were significantly elevated in new-T2DM patients compared with healthy controls. Whether expression of circulating miRNA-146a holds predictive value for T2DM warrants further investigations.
    PLoS ONE 09/2013; 8(9):e73272. DOI:10.1371/journal.pone.0073272 · 3.53 Impact Factor
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    ABSTRACT: Stress-inducible protein heme oxygenase-1(HO-1) is well-appreciative to counteract oxidative damage and inflammatory stress involving the pathogenesis of alcoholic liver diseases (ALD). The potential role and signaling pathways of HO-1 metabolite carbon monoxide (CO), however, is still remained unclear. To explore the precise mechanisms, ethanol-dosed adult male Balb/c mice (5.0g/kg.bw.) or ethanol-incubated primary rat hepatocytes (100mmol/L) were pretreated by tricarbonyldichlororuthenium (II) dimmer (CORM-2, 8mg/kg for mice or 20μmol/L for heaptocytes), as well as other pharmacological reagents. Our data showed that CO released from HO-1 induction by quercetin prevented ethanol-derived oxidative injury, which was abolished by CO scavenger hemoglobin. The protection was mimicked by CORM-2 with the attenuation of GSH depletion, SOD inactivation, MDA overproduction, and the leakage of AST, ALT or LDH in serum and culture medium induced by ethanol. Moreover, CORM-2 injection or incubation stimulated p38 phosphorylation and suppressed abnormal Tnfa and IL-6, accompanying the alleviation of redox imbalance induced by ethanol and aggravated by inflammatory factors. The protective role of CORM-2 was abolished by SB203580 (p38 inhibitor) but not by PD98059 (ERK inhibitor) or SP600125 (JNK inhibitor). Thus, HO-1 released CO prevented ethanol-elicited hepatic oxidative damage and inflammatory stress through activating p38 MAPK pathway, suggesting a potential therapeutic role of gaseous signal molecule on ALD induced by naturally occurring phytochemicals.
    Toxicology and Applied Pharmacology 08/2013; 273(1). DOI:10.1016/j.taap.2013.08.019 · 3.63 Impact Factor
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    ABSTRACT: Our aim was to study whether there is causal association between serum uric acid and metabolic syndrome (MetS). A cross-sectional study was performed, including a total of 27,009 subjects (23,345 subjects having uric acid data) from the Dongfeng-Tongji Cohort study. The MetS was defined by the International Diabetes Foundation criteria of 2005. Association analysis was performed by logistic regression. A genetic risk score was calculated by adding the uric acid increasing alleles in two SNPs (rs11722228 in SLC2A9 and rs2231142 in ABCG2) which were identified from our genome-wide association study on uric acid levels. The causal association was examined by mendelian randomization analysis. Among a middle- and old-age Chinese population, serum uric acid concentrations were strongly associated with the risk of MetS and its several components (P < 0.0001). The effects were stronger in women than in men. Despite the lack of statistical significance, both SNPs exhibited a trend with increased MetS risk (rs11722228, OR = 1.06, 95 % CI 0.99-1.14; rs2231142, OR = 1.02, 95 % CI 0.95-1.10), consistent with their increasing uric acid effects. Each additional uric acid increasing allele in the genetic risk score was associated with 3 % increased MetS risk (OR = 1.03, 95 % CI 0.98-1.09; P = 0.23). Further adjustment for serum uric acid attenuated the trend of individual SNP and genetic risk score with increased MetS risk (all OR < 1.0). These findings suggested that serum uric acid was associated with MetS risk in a middle- and old-age Chinese population. Whether this association was causal remained to be investigated in the future studies.
    European Journal of Epidemiology 07/2013; DOI:10.1007/s10654-013-9829-4 · 5.15 Impact Factor