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  1. AU="Beibei, Tao"
  2. AU="Lu, Kaifeng"
  3. AU="Hamade, Aline"
  4. AU="Pereira, Rickson"
  5. AU="Zou, Binbin"
  6. AU="Peng, Lingteng"
  7. AU="Zolotoukho, Anna"
  8. AU="Verhagen, E."
  9. AU=Butters Desley AU=Butters Desley
  10. AU="Hoffmann, Karl-Titus"
  11. AU="Iñiguez, Andrés"
  12. AU="Panaccione, Alexander"
  13. AU="Berube, Liliana L"

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  1. Artikel ; Online: Qi-Zhu-Xie-Zhuo-Fang reduces serum uric acid levels and ameliorates renal fibrosis in hyperuricemic nephropathy rats.

    Huijuan, Wang / Xiaoxu, Chen / Rui, Song / Xinghui, Li / Beibei, Tao / Jianchun, Mao

    Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie

    2017  Band 91, Seite(n) 358–365

    Abstract: Hyperuricemia is associated with the development of chronic kidney disease. Epithelial-to-mesenchymal transition (EMT) induced by hyperuricemia is blamed for initiation of renal fibrosis, which is one of the main characters of hyperuricemic nephropathy. ... ...

    Abstract Hyperuricemia is associated with the development of chronic kidney disease. Epithelial-to-mesenchymal transition (EMT) induced by hyperuricemia is blamed for initiation of renal fibrosis, which is one of the main characters of hyperuricemic nephropathy. Qi-Zhu-Xie-Zhuo-Fang (QZXZF) has been employed clinically for many years to treat patients with hyperuricemic nephropathy, but the mechanism underlying the therapeutic potential remains unclear. In the present study, QZXZF was applied to rats treated with adenine (100mg/kg) and potassium oxonate (300mg/kg) and biochemical estimations, morphology and immunohistochemistry were performed to investigate whether QZXZF can improve hyperuricemia induced renal fibrosis and to explore the possible mechanisms. We found QZXZF significantly reduced serum uric acid, cystatinC and hepatic xanthine oxidase (XO) activities, meanwhile improved renal histopathologic changes of hyperuricemic nephropathy rats. Furthermore, QZXZF not only substantially decreased the protein levels of fibronectin and Collagen I but also downregulated E-cadherin and upregulated α-SMA in the kidneys of hyperuricemic nephropathy rats. In conclusion, QZXZF reduced serum uric acid levels and protected kidney against fibrosis in potassium oxonate and adenine induced hyperuricemic nephropathy rats. The mechanism might be associated with the inhibition of hepatic XO activity and the renal epithelial-to-mesenchymal transition.
    Sprache Englisch
    Erscheinungsdatum 2017-07
    Erscheinungsland France
    Dokumenttyp Journal Article
    ZDB-ID 392415-4
    ISSN 1950-6007 ; 0753-3322 ; 0300-0893
    ISSN (online) 1950-6007
    ISSN 0753-3322 ; 0300-0893
    DOI 10.1016/j.biopha.2017.04.031
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: Fatty-acid receptor CD36 functions as a hydrogen sulfide-targeted receptor with its Cys333-Cys272 disulfide bond serving as a specific molecular switch to accelerate gastric cancer metastasisResearch in context

    Rui Wang / Beibei Tao / Qilin Fan / Shengyue Wang / Li Chen / Junjie Zhang / Yinfang Hao / Shuang Dong / Zhe Wang / Wei Wang / Yixi Cai / Xutong Li / Tuvshin Bao / Xiaohui Wang / Xiaoming Qiu / Kekun Wang / Xinyu Mo / Yuqi Kang / Zhirong Wang

    EBioMedicine, Vol 45, Iss , Pp 108-

    2019  Band 123

    Abstract: Background: Hydrogen Sulfide (H2S), a third member of gasotransmitter family along with nitric oxide (NO) and carbon monoxide (CO), exerts a wide range of cellular and molecular actions in our body. There is a large body of evidence suggesting that H2S ... ...

    Abstract Background: Hydrogen Sulfide (H2S), a third member of gasotransmitter family along with nitric oxide (NO) and carbon monoxide (CO), exerts a wide range of cellular and molecular actions in our body. There is a large body of evidence suggesting that H2S plays an important role in cancer metastasis; however, the molecular mechanisms of H2S-mediated acceleration of cancer metastasis remain unknown. Methods: We examined the promote effects of H2S on phenotype of gastric cancer (GC) cells (including those of express wild type CD36 and mutant CD36) in vitro and in vivo. GC patients' samples were used for clinical translational significance evaluation. Findings: H2S triggered lipid metabolism reprogramming by significantly up-regulating the expression of the fatty-acid receptor CD36 (CD36) and directly activating CD36 in GC cells. Mechanistically, a disulfide bond located between cysteine (Cys)333 and Cys272 within the CD36 protein structure that was labile to H2S-mediated modification. The long chain-fatty acid (LC-FA) binding pocket was capped by a turn in the CD36 protein, located between helical and sheet structures that were stabilized by the Cys333-Cys272. This limited the secondary binding between LC-FAs and lysine (Lys)334. Breaking the Cys333-Cys272 disulfide bond restored the second LC-FA binding conformation of CD36. Targeting CD36 in vivo blocked H2S-promoted metastasis and improved animal survival. Interpretation: These findings identify that the Cys333-Cys272 disulfide bond disrupted the integrity of the second LC-FA binding conformation of CD36. Therefore, CD36 can directly activate LC-FA access to the cytoplasm by acting as a direct target molecule for H2S. Keywords: H2S, CD36, Disulfide bond, Long chain-fatty acid, Nrf2, Metastasis
    Schlagwörter Medicine ; R ; Medicine (General) ; R5-920
    Thema/Rubrik (Code) 571
    Sprache Englisch
    Erscheinungsdatum 2019-07-01T00:00:00Z
    Verlag Elsevier
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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