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  1. Article ; Online: Pen Yan Jing Tablets Alleviates Pelvic Inflammatory Disease by Inhibiting Akt/NF-κB Pathway.

    Tang, Ping / Ding, Qi / Lin, Juan / Yang, Xinrong / Wang, Yiting / Liu, Fangle / Zheng, Yuying / Lin, Liuqing / Wang, Deqin / Lin, Baoqin

    International journal of medical sciences

    2023  Volume 20, Issue 11, Page(s) 1386–1398

    Abstract: Purpose: ...

    Abstract Purpose:
    MeSH term(s) Humans ; Female ; Rats ; Animals ; NF-kappa B/metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; Signal Transduction ; NF-KappaB Inhibitor alpha/metabolism ; Tumor Necrosis Factor-alpha/metabolism ; Pelvic Inflammatory Disease/drug therapy ; Lipopolysaccharides/pharmacology ; Interleukin-6 ; Intercellular Adhesion Molecule-1/metabolism ; Vascular Cell Adhesion Molecule-1/metabolism ; Vascular Cell Adhesion Molecule-1/pharmacology ; Cyclooxygenase 2/metabolism
    Chemical Substances NF-kappa B ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; NF-KappaB Inhibitor alpha (139874-52-5) ; Tumor Necrosis Factor-alpha ; Lipopolysaccharides ; Interleukin-6 ; Intercellular Adhesion Molecule-1 (126547-89-5) ; Vascular Cell Adhesion Molecule-1 ; Cyclooxygenase 2 (EC 1.14.99.1)
    Language English
    Publishing date 2023-09-04
    Publishing country Australia
    Document type Journal Article
    ZDB-ID 2151424-0
    ISSN 1449-1907 ; 1449-1907
    ISSN (online) 1449-1907
    ISSN 1449-1907
    DOI 10.7150/ijms.87433
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Protective Role of Endothelial SIRT1 in Deep Vein Thrombosis and Hypoxia-induced Endothelial Dysfunction Mediated by NF-κB Deacetylation.

    Tang, Ping / Wang, Yiting / Yang, Xinrong / Wu, Zhongrui / Chen, Wenpei / Ye, Yuxin / Jiang, Yong / Lin, Liuqing / Lin, Bingqing / Lin, Baoqin

    Inflammation

    2023  Volume 46, Issue 5, Page(s) 1887–1900

    Abstract: Venous hypoxia is considered as the major pathogenetic mechanism linking blood flow stagnancy with deep vein thrombosis (DVT). Our previous study showed that activating SIRT1 may attenuate inferior vena cava (IVC) stenosis-induced DVT in rats. This study ...

    Abstract Venous hypoxia is considered as the major pathogenetic mechanism linking blood flow stagnancy with deep vein thrombosis (DVT). Our previous study showed that activating SIRT1 may attenuate inferior vena cava (IVC) stenosis-induced DVT in rats. This study was aimed to investigate the role of endothelial SIRT1 in DVT and hypoxia-induced endothelial dysfunction as well as the underlying mechanism. Protein profiling of IVCs and blood plasma of DVT rats induced by IVC stenosis was analysed by 4D Label free proteomics analysis. To verify the independent role of SIRT1 in DVT and oxygen-glucose deprivation (OGD)-induced endothelial dysfunction, SIRT1 specific activator SRT1720 and SIRT1 knockdown in both local IVCs and endothelial cells were employed. Moreover, the role of the NF-κB were investigated using NF-κB inhibitor caffeic acid phenethyl ester (CAPE). SRT1720 significantly inhibited thrombus burden, leukocytes infiltration, protein expressions of cell adhesion molecules and chemokines, as well as acetylation level of NF-κB/p65 in wild DVT rats, while these protective effects of SRT1720 were abolished in rats with SIRT1 knockdown in local IVCs. In vitro, SRT1720 protected endothelial cells against OGD-induced dysfunction characterized with enhanced adhesion of monocytes as well as the protein expressions of cell adhesion molecules and chemokines, whereas these protective effects of SRT1720 were vanished by SIRT1 stable knockdown. Furthermore, CAPE attenuated endothelial cell dysfunction and abolished these effects of SIRT1 knockdown. Collectively, these data suggested that endothelial SIRT1 plays an independent role in ameliorating hypoxia-induced endothelial dysfunction and thrombotic inflammation in DVT, and this effect is mediated by NF-κB deacetylation.
    MeSH term(s) Animals ; Rats ; Cell Adhesion Molecules ; Chemokines ; Constriction, Pathologic ; Endothelial Cells/metabolism ; Hypoxia/complications ; NF-kappa B/metabolism ; Sirtuin 1/metabolism ; Vascular Diseases ; Venous Thrombosis/metabolism ; Venous Thrombosis/pathology
    Chemical Substances Cell Adhesion Molecules ; Chemokines ; NF-kappa B ; Sirtuin 1 (EC 3.5.1.-) ; Sirt1 protein, rat (EC 3.5.1.-)
    Language English
    Publishing date 2023-06-24
    Publishing country United States
    Document type Journal Article
    ZDB-ID 434408-x
    ISSN 1573-2576 ; 0360-3997
    ISSN (online) 1573-2576
    ISSN 0360-3997
    DOI 10.1007/s10753-023-01848-9
    Database MEDical Literature Analysis and Retrieval System OnLINE

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