bluuebunny/crossref_metadata_2025_split huggingface dataset:
Mulberry leaves protect rat tissues from immobilization stress‐induced inflammation
Authors: Lee Chooi Yeng , Cheng Hwee Ming , Sim Si Mui 
Published: December 2008

AbstractThe ability of the antioxidants in the mulberry leaves to protect Sprague‐Dawley rats from injuries caused by immobilization stress was studied as an indicator of the tissue bioavailability of antioxidants. Nitrite level, lipid peroxidation and total antioxidant activity (TAA) in the plasma and tissues were measured. There were hypertrophy of the adrenal glands and kidneys, significant increased levels of nitrite in the plasma and adrenal glands, elevated thiobarbituric acid reactive substances (TBARS) in the plasma, kidneys and spleen, and a reduction of TAA in the plasma, liver, adrenal glands, kidneys and spleen of the immobilized rats. Antioxidants in the mulberry leaf extract suppressed the increase of nitrite and TBARS. Adrenal glands appeared to be the target organ of the antioxidants in the leaf extract. The low dose mulberry antioxidants were more effective than pure rutin (4 mg/day) to protect the cells against inflammation and peroxidation induced by stress.
Antioxidative and cytoprotective effects of Artemisia capillaris fractions
Authors: Hong Jung‐Hee , Lee Ji‐Won , Park Jung‐Hyun , Lee In‐Seon 
Published: December 2008

AbstractThe antioxidant effects of Artemisia capillaris fractions against reactive oxygen species (ROS) were evaluated by measuring scavenging activities against 1,1‐diphenyl‐2‐picrylhydrazyl (DPPH) radical, superoxide (O ), hydroxyl (HO·) and 2 nitric oxide (NO·) radical. Among five solvent fractions, ethyl acetate fraction showed the highest total polyphenol and total flavonoid contents as 648.75 and 89.09 μg/mg, respectively. Also, the ethyl acetate fraction showed the highest scavenging activity; the 50% inhibitory concentration (IC50, μg/mg) value for DPPH, O, HO· and NO· radical scavenging were 4.76, 31.54, 69.34 and 74.63, respectively. Additionally, the highest inhibition of rat liver microsomal lipid peroxidation was observed by ethyl acetate fraction. Except for free radical‐mediated protein damage, ethyl acetate fraction showed the highest scavenging activity. The effect of Artemisia capillaris fractions on cell viability and DNA damage induced by H2O2 in Raw 264.7 cell were also evaluated by MTT and comet assay, respectively. The protective effect of ethyl acetate fraction, as indicated by cell viability increasing 71% and DNA breakage decreasing 51% as compared with H2O2 ‐treated positive control. These results suggest that ethyl acetate fraction possess significant ROS scavenging and protective effect against oxidative DNA damage.
Oxidation of glutathione and superoxide generation by inorganic and organic selenium compounds
Authors: Chen Jau‐Jiin , Boylan L. Mallory , Wu Chih‐Kang , Spallholz Julian E. 
Published: December 2008

AbstractThe carcinostatic activities of selenium (Se) compounds have been shown to be composition and concentration dependent. Several studies have indicated that the ratios between glutathione (GSH) and Se may play an important role in Se catalysis and toxicity. The present study examined the catalytic effect of three selenium compounds on GSH oxidation using lucigenin‐dependent chemiluminescence (CL) as an indirect measure of superoxide generation. Various GSH:Se ratios were assayed for the glutathione oxidase activity of selenite, selenocystamine and diselenodipropionic acid. CL emitted from the reaction of selenite with GSH increased more rapidly and was greater than those from the diselenides, but the diselenide CL reactions were sustainable. Both selenite‐ and diselenide‐induced CL were markedly suppressed by superoxide dismutase (SOD). Iodoacetic acid (IAc) effectively inhibited CL generated from selenite‐, selenocystamine‐ and diselenodipropionic acidcatalyzed GSH oxidation. These results suggest that GSH oxidation catalyzed by selenite, and the diselenides selenocystamine and diselenodipropionic acid, generated the superoxide radical in which the CL was inhibited by SOD. Furthermore, CL inhibition by IAc suggests that the catalytic species producing superoxide were the GSSe− or RSe− anion. This redox chemistry may be responsible for selenite and organoselenium toxicity and apoptosis, making possible the design and synthesis of organoselenium‐containing pharmaceuticals.
Pregnenolone and dexamethasone, modulators of cytochrome P450‐3A, not increase but reduce urinary α‐CEHC excretion in rats
Authors: Li Yi‐Jen , Shaw Huey‐Mei 
Published: December 2008

AbstractIn this study, the CYP3A inducer pregnenolone‐16α‐carbonitrile (PCN) and the CYP3A inhibitor ketoconazole (KCZ) were used to investigate whether the metabolism of α‐tocopherol to its metabolite, α‐carboxyethyl hydroxychroman (α‐CEHC), is CYP3A‐dependent in rats. In experiment 1, two groups of Wistar rats were fed for 3 wk with either a basal diet (containing 50 ppm of α‐tocopherol) or the same diet containing 10‐fold more α‐tocopherol. In the last 3 days, each group was divided into 2 subgroups which were given a single i.p. injection of either PCN at 75 mg/kg/d (P50 & P500 groups) or DMSO (D50 & D500 groups). The liver TBARS concentration was highest in the P50 group. Two‐way ANOVA analysis showed that α‐tocopherol levels in the plasma and liver were both significantly decreased by PCN (p < 0.0001), as were α‐CEHC levels in the urine (p = 0.0004). In experiment 2, α‐tocopherol levels in the liver were increased and α‐CEHC excretion in the urine decreased in the Wistar rats fed with KCZ containing diet. In experiment 3, Wistar rats administered with dexamethasone (DEX) significantly decreased α‐tocopherol levels in the plasma and liver and α‐CEHC levels in the urine. These data showed CYP3A is not a major contributor of the metabolism of α‐tocopherol to α‐CEHC. Nevertheless, vitamin E status was markedly reduced by CYP3A inducers due to increased lipid peroxidation and this would increase the consumption of α‐tocopherol in the liver.
Survival rate of preantral follicles derived from vitrified neonate mouse ovarian tissue by cryotop and conventional methods
Authors: Eimani H. , Mamzoji S. S. , Soleimani M. M. , Abnosi M. H. , Valojerdi M. Rezazadeh , Yazdi P. Eftekhari , Shahverdi A. , Guorabi H. 
Published: December 2008

AbstractThe aim of this study was to investigate the growth and survival rate of preantral follicles isolated from vitrified ovarian tissue by Cryotop and conventional methods. The ovaries of 14‐day‐old mice were separated and divided into four groups as following: Cryotop group, vitrified by Cryotop; CV (Conventional; CV) group, vitrified by conventional straw; toxicity test group and control group. After warming the vitrified ovaries, isolated preantral follicles from four groups were cultured for 4 days to compare survival rate and follicular growth between above‐mentioned groups. Survival rate (97.3%) in toxicity test group alike the control group (98.7%) were significantly higher (P < 0.05) than the Cryotop (92.7%) and CV (47.7%) groups. Increase in follicle diameters after 4 days in Cryotop and CV groups was significantly lower (P < 0.05) than the control and toxicity test groups, but growth and survival rate of follicles in Cryotop group was significantly higher (P < 0.05) than the CV group. These results demonstrated that ovarian tissue vitrification by Cryotop highly preserves the viability rate of preantral follicles.
Serum selenium concentration in healthy children living in Tehran
Authors: Safaralizadeh Reza , Sirjani Mahshid , Pourpak Zahra , Kardar Gholamali , Teimourian Shahram , Shams Sedigheh , Namdar Zahra , Kazemnejad Anoushiravan , Moin Mostafa 
Published: December 2008

AbstractIntroduction: Selenium is one of the essential trace elements which is more notifed in children in recent years. Reliable age‐specifc reference values for selenium in children in Iran are not clear and are important for the identifcation of selenium defciency and some other researches that is the aim of this study.Methods: Serum samples of 216 healthy children were analyzed by using hydride generation and flame atomic absorption spectroscopy to measured selenium level.Results: The mean and standard deviation of serum selenium level in children 0–16 years old (mean: 39.83 months) was 72.14 ± 16.80 μg/l. There was signifcant difference in serum selenium concentration between two sexes which was 76.78 ± 15.24 μg/l and 69.56 ± 17.09 μg/l in girls and boys respectively (P value = 0.002 ). There was also a positive correlation between higher selenium serum concentration and age in both sexes.Conclusion: Essential trace element's normal ranges are fundamental data which could use in many studies. Serum selenium concentration in healthy Iranian children that found in this study is very close to serum concentration of European children. Our fndings may reveal nutritional culture's similarity.
Gene expression in arcuate nucleus‐median eminence of rats treated with leptin or ciliary neurotrophic factor
Authors: Ambati Suresh , Duan Jiuhua , Duff Emily , Choi Yang‐Ho , Hartzell Diane L. , Della‐Fera Mary Anne , Baile Clifton A. 
Published: December 2008

AbstractCiliary neurotrophic factor (CNTF) and leptin are cytokine‐like hormones and act on their corresponding receptors in the hypothalamic arcuate nucleus (ARC). The present study was designed to assess effects of intracerebroventricular (ICV) injection of leptin and CNTF on gene expression in micropunched hypothalamic arcuate nucleus‐median eminence (ARCME) complex samples from rats. Male Sprague Dawley rats were implanted with lateral cerebroventricular cannulas for administration of control, 10 μg/d leptin or 5 μg/d CNTF for four days. Real‐time Taqman RT‐PCR was used to quantitatively compare the mRNA levels of selected genes in the ARC‐ME complex. Leptin and CNTF increased ARC‐ME mRNA levels of signal transducer and activator of transcription 3 (STAT3) by 64.5 and 124.7% (p < 0.01), suppressor of cytokine signaling 3 (SOCS3) by 258.9 and 1063.9% (p < 0.01), cocaine and amphetamine regulated transcript (CART) by 102.7 and 123.1% (p < 0.01), and proopiomelanocortin (POMC2) by 374.1 and 264.9% (p < 0.01), respectively. Leptin increased growth hormone releasing hormone (GHRH) by 309.9% (p < 0.01), while CNTF increased janus kinase 2 (JAK2) mRNA by 31.7% (p < 0.01) and decreased gonadotropin releasing hormone 1 (GNRH1) by 59.7% (p < 0.01), mitogen activated protein kinase 1 (MAPK1) by 19.4% (p < 0.05) and tyrosine hydroxylase (TH) by 74.5% (p < 0.05). Significant reduction in daily food intake and body weights by both the treatments was observed. Also, decrease in weights of fat pads was concomitant with lowered serum insulin and leptin levels. Our findings show that leptin and CNTF engage both convergent and divergent pathways involved in feeding, cellular signaling, inflammation, and other related regulatory systems.
NTPDase and 5'‐nucleotidase activities in physiological and disease conditions: New perspectives for human health
Authors: Schetinger Maria Rosa C. , Morsch Vera Maria , Bonan Carla Denise , Wyse Angela T. S. 
Published: December 2008

AbstractExtracellular nucleotides and nucleosides act as signaling molecules involved in a wide spectrum of biological effects. Their levels are controlled by a complex cell surface‐located group of enzymes called ectonucleotidases. There are four major families of ectonucleotidases, nucleoside triphosphate diphosphohydrolases (NTPDases/CD39), ectonucleotide pyrophosphatase/phosphodiesterases (E‐NPPs), alkaline phosphatases and ecto‐5'‐nucleotidase. In the last few years, substantial progress has been made toward the molecular identification of members of the ectonucleotidase families and their enzyme structures and functions. In this review, there is an emphasis on the involvement of NTPDase and 5'‐nucleotidase activities in disease processes in several tissues and cell types. Brief background information is given about the general characteristics of these enzymes, followed by a discussion of their roles in thromboregulatory events in diabetes, hypertension, hypercholesterolemia and cancer, as well as in pathological conditions where platelets are less responsive, such as in chronic renal failure. In addition, immunomodulation and cell‐cell interactions involving these enzymes are considered, as well as ATP and ADP hydrolysis under different clinical conditions related with alterations in the immune system, such as acute lymphoblastic leukemia (ALL), Bchronic lymphocytic leukemia (B‐CLL) and infections associated with human immunodeficiency virus (HIV). Finally, changes in ATP, ADP and AMP hydrolysis induced by inborn errors of metabolism, seizures and epilepsy are discussed in order to highlight the importance of these enzymes in the control of neuronal activity in pathological conditions. Despite advances made toward understanding the molecular structure of ectonucleotidases, much more investigation will be necessary to entirely grasp their role in physiological and pathological conditions.
Amadori‐glycated albumin‐induced vascular smooth muscle cell proliferation and expression of inhibitor of apoptosis protein‐1 and nerve growth factor‐γ
Authors: Lee Byung‐Wan , Ihm Jahei , Kang Jun Gu , Choi Moon Gi , Yoo Hyung Joon , Ihm Sung‐Hee 
Published: December 2008

AbstractWe investigated the effects of Amadori‐glycated serum albumin (GSA) on cell proliferation as well as expressions of antioxidant enzyme genes and marker genes associated with signal transduction pathways in rat aortic vascular smooth muscle cells (VSMCs). Quiescent VSMCs treated with GSA (0–500 μg/mL, 48 h) exhibited a dose‐dependent increase in proliferation that was prevented by PD98059 (25 μM), suggesting a MAPK‐dependent signaling pathway. Compared with bovine serum albumin (BSA)‐treated cells, the GSA (500 μg/mL, 24 h)‐treated VSMCs showed a higher superoxide dismutase 2 gene expression in quantitative RT‐PCR, suggesting the involvement of oxidative stress. In a focused oligonucleotide array containing 96 signal transduction‐related genes, expression of inhibitor of apoptosis protein‐1 (IAP‐1), nerve growth factorγ (NGF‐γ), and c‐jun genes was significantly higher in the GSA‐treated VSMCs. These results suggest that induction of antiapoptotic proteins like IAP‐1 and strong mitogens like NGF‐γ by GSA might further contribute to the VSMC proliferation and accelerated vascular remodeling in diabetes.
Selenium is critical for cancer‐signaling gene expression but not cell proliferation in human colon Caco‐2 cells
Authors: Zeng Huawei , Botnen James H. 
Published: December 2008

AbstractSelenium (Se) is a potential anticarcinogenic nutrient, and the essential role of Se in cell growth is well recognized but certain cancer cells appear to have acquired a survival advantage under conditions of Se‐deficiency. To understand the molecular basis of Se‐anticancer effects at nutritional doses (nmol/L) for cultured cells, we generated Se‐deficient colon Caco‐2 cells by gradually reducing serum in media because serum contains a trace amount of Se. The glutathione peroxidase (GPx) activity of Se‐deficient Caco‐2 cells was 10.8 mU/mg protein compared to 133.6 ∼146.3 mU/mg protein in Caco‐2 cells supplemented with 500 nmol/L selenite, SeMSC or SeMet (three tested Se‐chemical forms) after 7‐d culture in serum free media. Interestingly, there were no detectable differences in cell growth, cell cycle progression between Se‐deficient cells and cells supplemented with 500 nmol/L Se. To examine differential cancer signaling‐gene expression between Se‐deficient and Se‐supplemented cells, we employed a cancer signal pathway‐specific array assay coupled with the real time PCR analysis. Our data demonstrate that although Caco‐2 cells are resistant to Se deprivation, Se may exert its anticancer property through increasing the expression of humoral defense gene (A2M) and tumor suppressor‐related genes (IGFBP3, HHIP) while decreasing pro‐inflammatory gene (CXC L9, HSPB2) expression.
BTB/POZ domain of speckle‐type POZ protein (SPOP) confers proapoptotic function in HeLa cells
Authors: Byun Boohyeong , Tak Heejae , Joe Cheol O. 
Published: December 2008

AbstractThe proapoptotic function of SPOP protein was investigated in HeLa cells. HeLa cells underwent apoptosis by the overexpression of SPOP. Studies using SPOP deletion mutants suggest that BTB/POZ domain of SPOP protein is important for the induction of apoptosis in transfected cells. This study first proposes the proapoptotic aspect of the BTB/POZ domain of SPOP protein based on the finding that cells expressing the C‐terminal fragment of SPOP containing the BTB/POZ domain underwent apoptosis.
α‐Tocopherol counteracts ritonavir‐induced proinflammatory cytokines expression in differentiated THP‐1 cells
Authors: Guo Weimin , Zingg Jean Marc , Meydani Mohsen , Azzi Angelo 
Published: December 2008

AbstractTreatment of HIV‐infected individuals with HIV protease inhibitor (HPI) drugs has significantly increased their life span. However, one of the side effects of HPI drugs is the development of premature atherosclerosis, whose molecular pathogenesis remains unclear. Previously we have reported that α‐tocopherol (α‐T) normalizes CD36 overexpression induced by ritonavir treatment and reduces oxLDL uptake in THP‐1 cells. Since inflammation is a major player in the pathogenesis of atherosclerosis, we hypothesized that HPI drugs, such as ritonavir, increase proinflammatory cytokines synthesis and that α‐T supplementation counteracts this effect by suppressing proinflammatory cytokines levels. Here, we report that after differentiating THP‐1 cells to macrophages, ritonavir treatment (10 μg/mL) significantly increases expression of proinflammatory cytokines, IL‐6, MCP‐1 and IL‐8, at both mRNA and protein levels. This ritonavir‐induced effect is significantly suppressed by treatment of THP‐1/macrophages with 50 μM α‐T. We conclude that ritonavir can induce proinflammatory cytokines synthesis in THP‐1/macrophages, which might be associated with the development of premature atherosclerosis in ritonavir‐treated patients and that this effect is prevented by α‐T.
The influence of folic acid depletion on the Nucleotide Excision Repair capacity of human dermal fibroblasts measured by a modified Host Cell Reactivation Assay
Authors: Burger Katharina , Kieser Nicole , Gallinat S. , Mielke H. , Knott S. , Bergemann Jörg 
Published: December 2008

AbstractAnimal and human studies have shown that low levels of folic acid are associated with an impaired DNA Repair Capacity (DRC) and an increased cancer risk. However, the molecular evidence that folic acid enhances the DRC of cultured human cells is still limited because of a paucity of in vitro studies. We investigated the effect of folic acid depletion in vitro on the DRC of human dermal fibroblasts derived from 17 donors of different ages.To assess the cellular Nucleotide Excision DRC, we used a modified Host Cell‐Reactivation Assay (HCRA), adapted to the Fluorescence Activated Cell Sorting (FACS)‐technology, which is highly sensitive in comparison to luminometer‐technology and allows single cell based analysis. We used DsRed as a reporter (irradiated with UVC light) and pEGFP to control the performance of the transformations.Folic acid had a statistically significant effect on the DRC in all of the 17 donors, however, the levels varied considerably between individuals (2.0–19.6%).When the effect of folic acid substituted on the DRC was compared to donor age, we observed that there was less DNA repair in old donors compared to the younger donors, although this was only significant at lower levels.
Chaga mushroom extract inhibits oxidative DNA damage in lymphocytes of patients with inflammatory bowel disease
Authors: Najafzadeh Mojgan , Reynolds P. Dominic , Baumgartner Adolf , Jerwood David , Anderson Diana 
Published: December 2008

AbstractInflammatory Bowel Disease (IBD) is partly caused by oxidative stress from free radicals and reduced antioxidant levels. Using hydrogen peroxide to induce oxidative stress in vitro in peripheral lymphocytes we investigated the induction of DNA damage supplemented with ethanolic extract of Chaga mushroom as a protective antioxidant. Lymphocytes were obtained from 20 IBD patients and 20 healthy volunteers. For treatment, a constant H2 O2 dose (50 μg/ml) was used with variable doses of Chaga extract (10–500 μg/ml). DNA damage was evaluated in 50 cells per individual and dose using the Comet assay (making 1000 observations per experimental point ensuring appropriate statistical power). Chaga supplementation resulted in a 54.9% (p < 0.001) reduction of H2 O2 induced DNA damage within the patient group and 34.9% (p < 0.001) within the control group. Lymphocytes from Crohn's disease (CD) patients had a greater basic DNA damage than Ulcerative Colitis (UC) patients (p < 0.001). Conclusively, Chaga extract reduces oxidative stress in lymphocytes from IBD patients and also healthy individuals when challenged in vitro. Thus, Chaga extract could be a possible and valuable supplement to inhibit oxidative stress in general.
Antidiabetic and antioxidative effects of Annona squamosa leaves are possibly mediated through quercetin‐3‐O‐glucoside
Authors: Panda Sunanda , Kar Anand 
Published: December 2008

AbstractPresent investigation was made to reveal the involvement of a quercetin in the antidiabetic and antiperoxidative effects of Annona squamosa leaf extract.Quercetin‐3‐O‐glucoside (characterized by UV, IR, MS and NMR analyses) was isolated from Annona squamosa leaves and examined for its potential to regulate alloxan‐induced hyperglycemia and lipid peroxidation (LPO) in rats. While in alloxan treated animals, an increase in the concentration of serum glucose with a parallel decrease in insulin level was observed, administration of 15 mg/kg/day of isolated quercetin‐3‐O‐glucoside for 10 consecutive days to the hyperglycemic animals reversed these effects and simultaneously inhibited the activity of hepatic glucose‐6‐phosphatase. It further decreased the hepatic and renal LPO with a concomitant increase in the activities of antioxidative enzymes, such as catalase (CAT) and superoxide dismutase (SOD) and in glutathione (GSH) content, indicating its safe and antiperoxidative effects. These findings suggest the potential of quercetin‐3‐O‐glucoside in the amelioration of diabetes mellitus and tissue lipid peroxidation. It also appears that the antidiabetic effects of A. squamosa leaf extract is possibly mediated through the insulin stimulating and/or free radical scavenging properties of its active constituent, quercetin‐3‐O‐glucoside.
Influence of Coenzyme Q10 on release of pro‐inflammatory chemokines in the human monocytic cell line THP‐1
Authors: Schmelzer Constance , Lorenz Gerti , Rimbach Gerald , Döring Frank 
Published: December 2008

AbstractCoenzyme Q10 (CoQ10 ) is an obligatory element in the mitochondrial electron transport system and functions as a potent antioxidant of lipid membranes. In‐vivo and in‐vitro studies indicate an involvement of CoQ10 in inflammatory pathways. Here we studied in the human monocytic cell‐line THP‐1 the influence of CoQ10 on LPS‐induced secretion of the pro‐inflammatory chemokines Macrophage inflammatory protein‐1 alpha (MIP‐1α), Regulated upon activation, normal T cell expressed and secreted (RANTES) and Monocyte chemoattractant protein‐1 (MCP‐1). In comparison to unstimulated cells, LPS leads to 22‐, 3‐ and 4.5‐fold higher levels of MIP‐1α, RANTES and MCP‐1 in the cell culture medium, respectively. Pre‐incubation of cells with 10 μM CoQ10 resulted in a significant decrease of LPS‐induced MIP‐1α and RANTES secretion to 55.04% (p = 0.02) and 76.84% (p = 0.04), respectively. In conclusion, CoQ10 reduces the LPS‐induced secretion levels of the pro‐inflammatory chemokines MIP‐1α and RANTES in the human monocytic cell line THP‐1. These data suggest that CoQ10 possesses anti‐inflammatory properties.