يعرض 1 - 10 نتائج من 14 نتيجة بحث عن '"Lactate dehydrogenase"', وقت الاستعلام: 0.59s تنقيح النتائج
  1. 1
    دورية أكاديمية

    المصدر: Bioscience, Biotechnology & Biochemistry; Jan2022, Vol. 86 Issue 1, p47-55, 9p

    مستخلص: Nesfatin-1 is a neuropeptide produced in the hypothalamus. It is known that Nesfatin-1 is involved in food uptake, fat storage, and other metabolic regulation. We hypothesized that Nesfatin-1 may play a role in cardiovascular tissue. Free fatty acids (FFAs) are known to be the risk factor for cardiovascular diseases. FFA-mediated endothelial dysfunction is the critical mechanism of many cardiovascular disorders. The present study explores the protective effects of Nesfatin-1 on FFA-induced endothelial inflammation and the underlying mechanism. We found that significantly increased lactate dehydrogenase release and production of inflammatory factors were observed in FFA-treated human aortic endothelial cells (HAECs), accompanied by the enhanced attachment of U937 monocytes to HAECs and upregulated cell adhesion molecule vascular cell adhesion molecule-1, which were dramatically reversed by the treatment with Nesfatin-1. In addition, the promoted level of nuclear regulator NF-κB p65 and transcriptional function of NF-κB in FFA-treated HAECs were greatly suppressed by HAECs. Growth Factor Independent 1 Transcriptional Repressor 1 (Gfi1), an important negative regulator of NF-κB activity, was significantly downregulated in HAECs by FFAs and was upregulated by Nesfatin-1. Lastly, the inhibitory effects of Nesfatin-1 against FFA-induced NF-κB activation and adhesion of U937 monocytes to HAECs were abolished by the knockdown of Gfi1. In conclusion, our data reveal that Nesfatin-1 inhibited FFA-induced endothelial inflammation mediated by the Gfi1/NF-κB signaling pathway. [ABSTRACT FROM AUTHOR]

    : Copyright of Bioscience, Biotechnology & Biochemistry is the property of Oxford University Press / USA and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

  2. 2
    دورية أكاديمية

    المصدر: Bioscience, Biotechnology & Biochemistry; Oct2021, Vol. 85 Issue 10, p2185-2190, 6p

    مستخلص: Backhousia citriodora (lemon myrtle) extract has been found to inhibit glucansucrase activity, which plays an important role in biofilm formation by Streptococcus mutans. In addition to glucansucrase, various virulence factors in S. mutans are involved in the initiation of caries. Lactate produced by S. mutans demineralizes the tooth enamel. This study investigated whether lemon myrtle extract can inhibit S. mutans lactate production. Lemon myrtle extract reduced the glycolytic pH drop in S. mutans culture and inhibited lactate production by at least 46%. Ellagic acid, quercetin, hesperetin, and myricetin, major polyphenols in lemon myrtle, reduced the glycolytic pH drop and lactate production, but not lactate dehydrogenase activity. Furthermore, these polyphenols reduced the viable S. mutans cell count. Thus, lemon myrtle extracts may inhibit S. mutans -mediated acidification of the oral cavity, thereby preventing dental caries and tooth decay. [ABSTRACT FROM AUTHOR]

    : Copyright of Bioscience, Biotechnology & Biochemistry is the property of Oxford University Press / USA and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

  3. 3
    دورية أكاديمية

    المؤلفون: Qi, Mingxu, He, Li, Ma, Xiaofeng, Li, Zili

    المصدر: Bioscience, Biotechnology & Biochemistry; Jul2020, Vol. 84 Issue 7, p1353-1361, 9p

    مستخلص: MiR-181a-5p's mechanism in hypoxia–reoxygenation (H/R)-induced cardiomyocytes apoptosis has not been clarified. This study verified that SIRT1 was the target of miR-181a-5p. MiR-181a-5p expression was up-regulated or down-regulated in H/R-induced cardiomyocytes, and SIRT1 was transfected into cells alone or in combination with miR-181a-5p. Cell viability, apoptosis, levels of released lactate dehydrogenase (LDH), malondialdehyde (MDA), and superoxide dismutase (SOD), as well as the Bcl-2, Bax, and Caspase 3 levels in treated cells were tested. On the one hand, down-regulated miR-181a-5p promoted cell viability, reduced released LDH and MDA, and increased SOD level in H/R-induced cardiomyocytes. On the other hand, miR-181a-5p inhibited apoptosis and elevated Bcl-2 expression while decreasing the expressions of Bax and Caspase 3 in treated cells, but the effects of miR-181a-5p could be rescued by SIRT1. In conclusion, miR-181a-5p involved in H/R-induced cardiomyocytes apoptosis through regulating SIRT1, which might become a novel direction for related diseases. SIRT1 counteracted the effects of over-expressed miR-181a-5p on hypoxia/reoxygenation (H/R)-induced cardiomyocytes. H/R: hypoxia–reoxygenation; qRT-PCR: quantitative reverse transcription-polymerase chain reaction; WB: western blot; MDA: malondialdehyde; LDH: lactate dehydrogenase; SOD: superoxide dismutase; AMI: Acute myocardial infarction; I/R: ischemia–reperfusion; DNA: Deoxyribonucleic acid; miRNAs: microRNA; mRNA: messenger RNAs; 3ʹ UTR: 3ʹ-untranslated region; NC: negative control; OD: optical density; PI: propidium iodide; PVDF: polyvinylidene fluoride [ABSTRACT FROM AUTHOR]

    : Copyright of Bioscience, Biotechnology & Biochemistry is the property of Oxford University Press / USA and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

  4. 4
    دورية أكاديمية

    المؤلفون: You, Sohyeon, Kim, Gun-Hee

    المصدر: Bioscience, Biotechnology & Biochemistry; Oct2019, Vol. 83 Issue 10, p1893-1900, 8p

    مستخلص: This study was undertaken to investigate the neuroprotective effect of an ethanolic extract of Mori Cortex radicis (MCR) against high glucose (HG)-induced oxidative damage in PC12 cells. Cell cytotoxicity was examined using MTT and lactate dehydrogenase assays. To examine the antioxidative effects, intracellular reactive oxygen species (ROS) and malondialdehyde (MDA) levels and the activities of antioxidant enzymes were measured. The expressions of apoptosis-associated proteins were assessed. MCR was found to increase the viabilities of HG-induced PC12 cells and to inhibit ROS and MDA production and to promote antioxidative enzyme activities. Furthermore, MCR reduced apoptosis by upregulating p-Akt and Bcl-2/Bax ratio and reducing cytochrome c level. The main flavonoids in MCR were identified by HPLC to be kuwanon G and morusin. These results suggest the antioxidative effects of MCR protect against HG-induced oxidative stress and that MCR has potential therapeutic use for the prevention and treatment of diabetic neuro-degeneration. Protective effect of MCR against HG-induced oxidative stress and its major compounds kuwanon G and morusin [ABSTRACT FROM AUTHOR]

    : Copyright of Bioscience, Biotechnology & Biochemistry is the property of Oxford University Press / USA and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

  5. 5
    دورية أكاديمية

    المصدر: Bioscience, Biotechnology & Biochemistry; Sep2019, Vol. 83 Issue 9, p1740-1746, 7p

    مستخلص: Sterol regulatory element-binding proteins (SREBPs) are transcription factors that regulate the expression of genes involved in fatty acid and cholesterol biosynthetic pathways. The present study showed that the flavonoid chrysin impairs the fatty acid synthase promoter. Chrysin reduces the expression of SREBP target genes, such as fatty acid synthase, in human hepatoma Huh-7 cells and impairs de novo synthesis of fatty acids and cholesterol. Moreover, it reduces the endogenous mature, transcriptionally active forms of SREBPs, which are generated by the proteolytic processing of precursor forms. In addition, chrysin reduces the enforced expressing mature forms of SREBPs and their transcriptional activity. The ubiquitin–proteasome system is not involved in the chrysin-mediated reduction of SREBPs mature forms. These results suggest that chrysin suppresses SREBP activity, at least partially, via the degradation of SREBPs mature forms. Abbreviations: ACC1: acetyl-CoA carboxylase 1; DMEM: Dulbecco's modified Eagle's medium; FAS: fatty acid synthase; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; 25-HC: 25-hydroxycholesterol; HMGCS: HMG-CoA synthase; LDH: lactate dehydrogenase; LPDS: lipoprotein-deficient serum; PI3K: phosphatidylinositol 3-kinase; SCD1: stearoyl-CoA desaturase; SREBPs: sterol regulatory element-binding proteins. Chrysin decreases the protein level of SREBPs mature forms regardless of the presence of MG132, a proteasome inhibitor. [ABSTRACT FROM AUTHOR]

    : Copyright of Bioscience, Biotechnology & Biochemistry is the property of Oxford University Press / USA and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

  6. 6
    دورية أكاديمية

    المؤلفون: Wu, Xing, Xu, Lin, Yan, Ming

    المصدر: Bioscience, Biotechnology & Biochemistry; Dec2016, Vol. 80 Issue 12, p2306-2310, 5p

    مستخلص: NAD + -dependent glyceraldehyde dehydrogenases usually had lower activity in the nonphosphorylated Entner–Doudoroff (nED) pathway. In the present study, a new NAD + -dependent glyceraldehyde dehydrogenase was engineered froml-lactaldehyde dehydrogenase ofE. coli(EC: 1.2.1.22). Through comparison of the sequence alignment and the active center model, we found that a residue N286 ofl-lactaldehyde dehydrogenase contributed an important structure role to substrate identification. By free energy calculation, three mutations (N286E, N286H, N286T) were chosen to investigate the change of substrate specificity of the enzyme. All mutants were able to oxidate glyceraldehyde. Especially, N286T showed the highest activity of 1.1U/mg, which was 5-fold higher than the reported NAD + -dependent glyceraldehyde dehydrogenases, and 70% activity was retained at 55 °C after an hour. Compared tol-lactaldehyde, N286T had a one-third lowerKmvalue to glyceraldehyde. Molecular structure ofl-lactaldehyde dehydrogenase fromE. coli. [ABSTRACT FROM PUBLISHER]

    : Copyright of Bioscience, Biotechnology & Biochemistry is the property of Oxford University Press / USA and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

  7. 7
    دورية أكاديمية

    المصدر: Bioscience, Biotechnology & Biochemistry; Sep2008, Vol. 72 Issue 9, p2448-2451, 4p, 1 Chart, 1 Graph

    مستخلص: The article focuses on the scientific content of lactate dehydrogenase A4 (LDH-A4). This was purified for yak skeletal muscle. Michaelis constant (Km) analysis showed that yak LDH-A4 for pyruvate was significantly higher than that of cattle, cDNA cloning of LDH-A revealed two amino acid substitutions between yak and cattle.

  8. 8
    دورية أكاديمية

    المصدر: Bioscience, Biotechnology & Biochemistry; Apr2014, Vol. 78 Issue 4, p651-654, 4p

    مصطلحات موضوعية: PIKAS, LACTATE dehydrogenase, CONTRACEPTIVE drugs, PROTEINS

    مصطلحات جغرافية: SICHUAN Sheng (China)

    مستخلص: The article studies inhibitor screening of lactate dehydrogenase C4 (LDH-C4) using black-lipped pika found in the Western Sichuan Plateau in Sichuan Province, China. It informs that LDH-C4 was found to be a good target protein for development contraceptive drugs. It states that screening inhibitors of pika LDH-C4 was carried out by virtual screening and in vitro enzyme assay.

  9. 9
    دورية أكاديمية

    المصدر: Bioscience, Biotechnology & Biochemistry; May2013, Vol. 77 Issue 5, p966-970, 5p

    مستخلص: The article discusses the results of a study which examines the formation of lactic acid from carbon dioxide in the atmosphere using lactate dehydrogenase genes in Synechocystis. It describes the use of several lactic acid-producing bacteria to engineer Synechocystis including Lactococcus lactis, Lactobacillus plantarum, and Lactobacillus rhamnosus. It mentions the secretion of lactic acid outside the cell by a transporter gene. Information on the expression of each bacteria is provided.

  10. 10
    دورية أكاديمية